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64 publications mentioning rno-mir-200c

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-200c. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 311
Similarly, MALAT1-silencing led to the upregulation of E-cadherin and the downregulation of ZEB1, ZEB2, and N-cadherin in HESCs; however, the cotransfection of these cells with the miR-200c inhibitor abolished E-cadherin upregulation and ZEB1, ZEB2, and N-cadherin downregulation. [score:15]
Functional studies showed that MALAT1 knockdown inhibits the proliferation and migration of HESCs, while downregulation of miR-200c expression restores these abilities in HESCs. [score:9]
We identified miR-200c as an EMT-suppressive miRNA in endometriosis that acts, at least in part, by downregulating the RNA level of MALAT1, which in turn functions as a ceRNA to upregulate ZEB1 and ZEB2 by sequestering miR-200c. [score:9]
EC ectopic endometrial, EN normal endometrial To better understand the biological function of miR-200c in endometriosis, primary endometrial stromal cells (HESCs) derived from human endometrial biopsies were transfected with the miR-200c mimic or inhibitor to overexpress or suppress miR-200c expression, respectively. [score:9]
EdU 5-ethynyl-2′-deoxyuridine, MALAT1 metastasis -associated lung adenocarcinoma transcript 1, Mimic NC negative control miRNA mimic, Inhibitor NC negative control miRNA inhibitor, siRNA small interfering RNA, siRNA NC negative control siRNA To investigate whether miR-200c is crucial for the progression of endometriosis in vivo, we established a rat endometriosis mo del to determine the effect of upregulation and downregulation of miR-200c. [score:9]
EdU 5-ethynyl-2′-deoxyuridine, Mimic NC negative control miRNA mimic, Inhibitor NC negative control miRNA inhibitor To gain insight into the mechanisms underlying the suppressive function of miR-200c in endometrial stromal cells, we next identified its target genes. [score:9]
In the current study, we found that miR-200c suppresses the proliferation and migration of endometrial stromal cells by downregulating metastasis -associated lung adenocarcinoma transcript 1 (MALAT1), a lncRNA which in turn functions as a miR-200c decoy and abolishes the suppressive effect of miR-200c. [score:8]
Further, western blot analysis confirmed the effect of the miR-200c inhibitor on expression of ZEB1, ZEB2, E-cadherin, and N-cadherin, and these changes in gene expression were reversed by MALAT1 knockdown (Fig.   4g). [score:8]
miR-200c suppresses expression of mesenchymal marker genes by downregulating MALAT1. [score:8]
g of ZEB1, ZEB2, N-cadherin, and E-cadherin expression after transfection of HESCs with the miR-200c inhibitor (100 nM), NC inhibitor, siMALAT1 (50 nM), or siNC for 48 hours. [score:7]
ZEB1 and ZEB2 mRNAs are well-described targets of the miR-200 family, and many reports have suggested that miR-200 family members block EMT by inhibiting ZEB1 and ZEB2 expression [15]. [score:7]
EC ectopic endometrial, EN normal endometrial, MALAT1 metastasis -associated lung adenocarcinoma transcript 1, Mimic NC negative control miRNA mimic, Inhibitor NC negative control miRNA inhibitor, siRNA small interfering RNA, siRNA NC negative control siRNA To define the role of miR-200c in the development and progression of endometriosis, we examined its effects on EMT regulation. [score:7]
g qRT-PCR analysis of MALAT1 expression in HESCs after transfection with the miR-200c mimic (50 nM), mimic NC, miR-200c inhibitor (100 nM), or inhibitor NC for 24 hours. [score:7]
Indeed, the overexpression of miR-200c increased the level of E-cadherin and decreased the levels of ZEB1, ZEB2, and N-cadherin proteins, whereas an opposite effect was observed when miR-200c was suppressed using the miR-200c inhibitor in HESCs. [score:7]
a of ZEB1, ZEB2, N-cadherin, and E-cadherin expression after transfection of HESCs with the miR-200c mimic (50 nM), NC mimic, miR-200c inhibitor (100 nM), or NC inhibitor for 48 hours. [score:7]
In addition, functional studies showed that overexpression of miR-200c inhibited the proliferation of HESCs, while the inhibition of miR-200c promoted cellular proliferation. [score:7]
Exogenous overexpression of miR-200c inhibited the proliferation and migration of HESCs, which were mainly regulated by metastasis -associated lung adenocarcinoma transcript 1 (MALAT1). [score:6]
As shown in Fig.   2a, b, Transwell assays revealed that miR-200c overexpression suppressed the migration of HESCs, whereas the opposite effect was observed when this miRNA was inhibited. [score:6]
The suppression of proliferation and migration by miR-200c therefore depends, to a certain extent, on the downregulation of MALAT1. [score:6]
To further investigate the correlation between miR-200c and MALAT1 expression in endometrial stromal cells, MALAT1 expression was knocked down in HESCs, which resulted in a significant increase in expression of miR-200c (Fig.   3h, i). [score:6]
In contrast, inhibition of miR-200c promoted the proliferation and migration of HESCs, while the simultaneous silencing of MALAT1 expression exerted the opposite effects. [score:5]
Moreover, functional studies showed that HESCs transfected with the miR-200c inhibitor demonstrated a significant increase in proliferation and migration; however, silencing of MALAT1 resulted in a significant reduction in proliferation and migration and abolished the effect of the miR-200c inhibitor on HESCs (Fig.   4c–f). [score:5]
e, f Relative luciferase activities in HESCs corresponding to binding site 1 (e) and binding site 2 (f) after cotransfection with the pMIR-REPORT-MALAT1 reporter and the miR-200c mimic (50 nM), mimic NC, miR-200c inhibitor (100 nM), or inhibitor NC for 48 hours. [score:5]
Therefore, miR-200c suppresses EMT by targeting MALAT1 in endometriosis. [score:5]
miR-200c overexpression resulted in a significant decrease in luciferase activity, whereas the opposite effect was observed when this miRNA was inhibited (Fig.   3e, f). [score:5]
Restoration of miR-200c expression in endometrial stromal cells suppresses cellular migration and proliferation. [score:5]
The mimic NC group and the miR-200c mimic group received 1 nmol RNA; the inhibitor NC group and the miR-200c inhibitor group received 2.5 nmol of RNA. [score:5]
We demonstrated that expression of MALAT1 in ectopic endometrial specimens was negatively correlated with that of miR-200c and that MALAT1 knockdown increased the level of miR-200c in HESCs. [score:4]
miR-200c directly targets the lncRNA MALAT1. [score:4]
Further, we conducted luciferase reporter assays and transfected cells with the miR-200c mimic or inhibitor to demonstrate that MALAT1 is a target of miR-200c in HESCs. [score:4]
miR-200c is frequently downregulated in endometriosis. [score:4]
Mechanistically, the MALAT1/miR-200c sponge acts, at least in part, by regulating expression of ZEB1 and ZEB2 in endometrial stromal cells. [score:4]
Near-infrared imaging showed that the intensity of fluorescence was significantly reduced in the miR-200c mimic treatment group compared with that in the mimic NC treatment group, while the intensity of fluorescence was significantly increased in the miR-200c inhibitor treatment group compared with that in the inhibitor NC treatment group (Fig.   5a, b). [score:3]
miR-200c has also been shown to be involved in the EMT through targeting ZEB1 and ZEB2, the transcriptional repressors of E-cadherin [15]. [score:3]
Therefore, miR-200c suppresses the migration and proliferation of endometrial stromal cells in vitro. [score:3]
Based on these findings, we used an miRNA–lncRNA interaction analysis program, starBase v2.0 [20], to screen for potential lncRNAs targeted by miR-200c. [score:3]
In contrast, the miR-200c inhibitor significantly promoted cell proliferation (Fig.   2c, d). [score:3]
In the present study, we found that miR-200c was significantly downregulated in EC compared with in EN tissues. [score:3]
The MALAT1/miR-200c sponge may be a potential therapeutic target for endometriosis. [score:3]
For in-vivo therapeutic interventions, polymeric nanoparticles of polyethylenimine–polyethylene glycol–arginine–glycine–aspartic acid were used for delivery of miR-200c mimic and inhibitor to determine the therapeutic effect of miR-200c in a rat mo del of endometriosis. [score:3]
b– d qPCR analysis of miR-200c (b), miR-638 (c), and let-7i (d) expression in 27 EC and 12 EN tissues. [score:3]
Furthermore, miR-200c mimic treatment reduced the volume of ectopic endometrial cysts, whereas miR-200c inhibitor treatment increased the volume of ectopic endometrial cysts in a rat endometriosis mo del. [score:3]
Therefore, MALAT1 is a target of miR-200c. [score:3]
In contrast, the miR-200c inhibitor significantly restored the MALAT1 RNA level in HESCs (Fig.   3g). [score:3]
In contrast, the miR-200c inhibitor significantly increased the protein levels of ZEB1 and ZEB2 in HESCs (Fig.   4a). [score:3]
Compared with those in EN tissues, three miRNAs (miR-200c, miR-638, and let-7i) were significantly downregulated in EC tissues (fold change cutoff ≥ 2.0 and P < 0.05) (Fig.   1a). [score:3]
As shown in Fig.   1b, miR-200c was significantly downregulated in EC tissues (n = 27) compared with in EN tissues (n = 12) (P < 0.0001). [score:3]
Overall, these findings suggest that the MALAT1/miR-200c sponge may represent a potential and novel therapeutic target for endometriosis. [score:3]
Two lncRNAs (MALAT1 and XIST) were identified as possible targets of miR-200c. [score:3]
The miR-200c mimic, miR-200c inhibitor, siRNA against MALAT1, and their respective negative controls (scrambled oligos) were obtained from RiboBio. [score:3]
When the rats were sacrificed 20 days after injection, we observed a significant reduction in the ectopic endometrial cyst volume in the miR-200c mimic treatment group compared with that in the mimic NC treatment group; in contrast, the volume of ectopic endometrial cysts was significantly increased in the miR-200c inhibitor treatment group compared with that in the inhibitor NC treatment group (Fig.   5c, d). [score:3]
miR-200c suppresses of the growth of endometriotic lesions in vivo. [score:3]
Furthermore, using a rat endometriosis mo del, we showed that local delivery of the miR-200c mimic significantly inhibited the growth of ectopic endometriotic lesions. [score:3]
The MALAT1/miR-200c sponge significantly affects the proliferation and migration of endometriotic stromal cells, indicating that this sponge may be a novel target for the diagnosis and treatment of endometriosis. [score:3]
In our study, we used a miRNA–lncRNA interaction analysis program and identified lncRNA MALAT1 and XIST as possible targets of miR-200c. [score:3]
Briefly, pMIR-REPORT-MALAT1 or pMIR-REPORT-MALAT1-mut was cotransfected with the miR-200c mimic, the miR-200c inhibitor, or the corresponding negative controls into HESCs using Lipofectamine 2000 according to the manufacturer’s instructions. [score:3]
In addition, we performed therapeutic interventions with the miR-200c mimic and inhibitor in a rat mo del of endometriosis, and our results demonstrated the potential therapeutic effect of miR-200c in endometriotic lesions. [score:3]
Moreover, the results of a 5-ethynyl-2′-deoxyuridine (EdU) incorporation assay indicated that miR-200c overexpression substantially reduced the rate of cell proliferation. [score:2]
These results suggested that MALAT1 regulated the proliferation and migration of HESCs in a miR-200c -dependent manner. [score:2]
c EdU assay to evaluate the proliferation of HESCs treated with the miR-200c inhibitor (100 nM), NC inhibitor, siMALAT1 (50 nM), or siNC for 48 hours (magnification, 200×). [score:2]
Moreover, mutations in the predicted miR-200c binding sites abolished this effect (Fig.   3d–f). [score:2]
e Transwell assay to evaluate the migration of HESCs treated with the miR-200c inhibitor (100 nM), NC inhibitor, siMALAT1 (50 nM), or siNC for 48 hours (magnification, 200×). [score:2]
The miR-200c binding sites at positions 3483 and 5466 containing partial MALAT1 sequences are located at 3410–3809 nt and 5205–5634 nt, respectively. [score:1]
In addition, miR-200c and MALAT1 levels were significantly negatively correlated. [score:1]
h, i Relative RNA levels of MALAT1 (h) and miR-200c (i) in HESCs that were transiently transfected with siMALAT1(50 nM) or siNC for 24 hours. [score:1]
c Pearson correlation analysis of miR-200c and MALAT1 RNA levels in EC tissues represented by Pearson R scores (n = 27, R < 0 denotes negative correlation). [score:1]
Of note, the miR200/MALAT1 sponge mediating the EMT processes in endometriosis is complex and never exclusive. [score:1]
Furthermore, the level of MALAT1 was significantly lower in cells transfected with the miR-200c mimic than in cells transfected with the negative control miRNA mimic (mimic NC) (Fig.   3g). [score:1]
Fig. 5Therapeutic delivery of miR-200c reduced ectopic endometrial cysts in a rat mo del. [score:1]
Therefore, miR-200c exerts a therapeutic effect in a rat mo del of endometriosis. [score:1]
Next, we used RNA hybridization programs to demonstrate that the MALAT1 sequence (NR_002819.2) contains two putative binding sites for miR-200c at 3483–3489 bp and 5466–5481 bp (Fig.   3d). [score:1]
An increase in miR-200c levels in HESCs by transfection of the miR-200c mimic repressed ZEB1 and ZEB2 protein levels (Fig.   4a). [score:1]
Moreover, the level of MALAT1 was negatively correlated with the miR-200c level (P < 0.0001, r = −0.8176) (Fig.   3c). [score:1]
These findings prompted us to look further into the role of miR-200c in endometriosis. [score:1]
Notably, endometrial stromal β-catenin is required for steroid -dependent mesenchymal–epithelial crosstalk and decidualization [33]; whether the LPAR3/β-catenin pathway also contributes to the EMT processes in endometriosis and its possible crosstalk with the miR200/MALAT1 sponge requires further research. [score:1]
Moreover, the transfection of endometrial stromal cells with the miR-200c mimic or MALAT1 siRNAs decreased the protein levels of mesenchymal markers ZEB1, ZEB2, and N-cadherin and increased the protein levels of the epithelial marker E-cadherin. [score:1]
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[+] score: 178
revealed negative expression correlation between miR-200 family and their target genesTo study how miR-200 family contributed to epididymal region-specific gene expression, we performed to examine whether putative target genes of miR-200 family were coordinately more or less expressed between caput and cauda epididymis. [score:11]
Given the higher expression of miR-200 family in the caput region, it was suggested that differentially expressed miR-200 family down-regulated their target genes in the epididymis. [score:10]
To study how miR-200 family contributed to epididymal region-specific gene expression, we performed to examine whether putative target genes of miR-200 family were coordinately more or less expressed between caput and cauda epididymis. [score:7]
The temporal and spatial manners of miR-200 family expression may contribute to epididymal development, regionalization and maintenance of function, as revealed by GO analysis that their target genes enriched in functions of anti-apoptosis, cell transportation and development. [score:7]
Among epididymal differentially expressed miRNAs, the whole miR-200 family was more expressed in the caput, compared with cauda, which inferred a role of this miRNA family in the maintenance of epididymal regional gene expression between the two physiologically distinct regions. [score:6]
We then studied and confirmed the negative expression correlation and bona fide regulation of miR-200 family on their target genes between caput and cauda. [score:6]
Comparatively, the miR-29 family showed consistent regional expression [25] while the miR-200 family were differentially expressed. [score:5]
Additionally, specific miRNAs such as miR-200a [26], miR-200c [27], miR-335 [28] and miR-29a [25] were identified to regulate epididymal development by targeting β-catenin, E-cadherin, Zeb1, Nasp and etc. [score:5]
All the 4 genes were more expressed in the cauda than caput (Fig 6B) based on the epididymal mRNA microarray data [31], and their 3’ UTR regions contained potential target sites of the miR-200 family, in whole or in part (Fig 6C). [score:5]
This result indicated that the putative miR-200 family target genes were significantly located in the bottom of the gene list and their expression in the cauda was statistically higher than in the caput. [score:5]
Right panel: heat map of miR-200 target gene expression in caput and cauda region (Cap1-5 and Cau1-6 reflected the subdivision of each region in the study performed by Jelinsky et al., [31]). [score:5]
Luciferase reporter assay was performed to verify the bona fide regulation of miR-200 family on 4 putative target genes (Bcap29, Rab21, Slc23a1 and Dek) whose 3’ UTR regions contained potential target sites of the 5 miRNAs, in whole or in part. [score:5]
Taken together, cauda expression of the miR-200 family were 30%- 70% lower than the caput level (Fig 4B), implicating potential roles of this miRNA family in maintaining region-specific gene expression between the two regions. [score:5]
Dual luciferase reporter assay was performed to confirm the targeting and regulation of miR-200 family on 4 predicted target genes: Bcap29, Rab21, Slc23a1 and Dek. [score:5]
Left panel: enrichment score of putative miR-200 target genes against their expression profile of caput and cauda epididymis. [score:5]
GSEA analysis revealed negative expression correlation between miR-200 family and their target genes. [score:5]
Bona fide regulation of miR-200 family on 4 putative target genesThe miR-200 family comprises of 5 miRNAs: miR-200a, miR-200b, miR-200c, miR-141 and miR-429. [score:4]
This result confirmed the bona fide interaction and regulation of miR-200 family to their targets. [score:4]
Interestingly, in these studies, the miR-200 family members tended to simultaneously up- or down-regulated in response to a certain change of physiological state [39, 46]. [score:4]
Functions of miR-200 family target genes were mainly enriched in the categories of “anti-apoptosis”(8.04%, P = 0.0002) (Ets1, Stat5a, Bnip3l, Tgfa, Nr3c1, Fn1, Cited2), “carboxylic acid transport”(6.90%, P = 0.0019) (Slc23a1, Slc38a2, Slc23a2, Serinc1, Slc6a15, Slco1a5), “transmembrane receptor protein tyrosine kinase signaling pathway”(6.90%, P = 0.0063) (Txnip, Flt1, Ndst1, Efna1, Stat5a, Tgfa) and “blood vessel development”(6.90%, P = 0.0126) (Flt1, Efna1, Tgfa, Ppap2b, Cxcl12, Cited2), suggesting that miR-200 family contributed to these functional diversities between caput and cauda epididymis. [score:4]
Bona fide regulation of miR-200 family on 4 putative target genes. [score:4]
In conclusion, our study revealed a role of region-specific epididymal miRNAs, especially the miR-200 family in regulating epididymal regional gene expression in adult rats, which might contribute to the distinct physiological function in sperm maturation / storage of caput / cauda epididymis. [score:4]
As two members of the miR-200 family (miR-200a and 141) were observed, we further examined the expression pattern of the remaining three miRNAs (miR-200b, 200c and 429). [score:3]
Among them, 5 miR-200 family miRNAs, together with miR-664 and miR-327, were shown by microarray to be differentially expressed between caput and cauda epididymis. [score:3]
Expression of both miR-200b and miR-200c were significantly higher in the caput (P<0.05) with around 2 fold in change and miR-429 was also higher in the caput, with P = 0.060 and fold change of 1.35. [score:3]
We performed GO enrichment analysis to further explore the potential functions of miR-200 family target genes. [score:3]
miR-200 family was more expressed in the caput than in the cauda epididymis. [score:3]
GO enrichment of miR-200 family target genes. [score:3]
Functional enrichment of miR-200 family target genes. [score:3]
Previous studies reported the epididymal temporal expression of miR-29and miR-200 families [25– 27]. [score:3]
As an important miRNA family, miR-200 miRNAs were proved to have marked biological significance in many aspects, especially in the inhibition of epithelial-mesenchymal transition (EMT) and repression of metastasis and progression of different cancer types such as ovarian and mammary cancer [39, 43– 46]. [score:3]
Results of GSEA analysis for target genes of miR-200 family. [score:3]
Result of GSEA analysis for miRNA-200 family target genes. [score:3]
0124450.g005 Fig 5 of for target genes of miR-200 family. [score:3]
Similarly, in our study, all 5 miR-200 family miRNAs showed higher expression in the caput (Fig 4B). [score:3]
As shown in Fig 5 and Table 4, for the miR-200 targets, their enrichment score achieved -2.01 with a significant P value (0.002) and FDR (0.9%, much less than 20%) when the parameter of “metric of ranking genes” was “diff_of_Classes” and the parameter of “Enrichment statistic” was “classic”. [score:3]
In this study, we verified Slc23a1, Rab21, Bcap29 and Dek as the bona fide targets of the miR-200 family. [score:3]
More detailed and specific actions of miR-200 family on epididymal development, sperm maturation and storage are needed to be explored in depth in the future studies. [score:2]
0124450.g004 Fig 4 (A) The expression of miR-200a, miR-200b, miR-200c, miR-141, miR-429, miR-664, miR-327 and let-7a was examined from the IS, Cap, Cor and Cau epididymis of 5 SD rats by qPCR and compared with microarray results. [score:2]
More specifically, channel proteins such as Slc23a1, Slc38a2, Slc23a2, Slc6a15 and Slco1a5 are under the regulation of miR-200 family. [score:2]
The miR-200 family comprises of 5 miRNAs: miR-200a, miR-200b, miR-200c, miR-141 and miR-429. [score:1]
Cells were transiently transfected with 100 ng of each of the above 4 constructs and together with respectively 40 pmol mimics of miR-200a, miR-200b, miR-200c, miR-141, miR-429 and miR-NC (Negative control miRNA, 5’- UUCUCCGAACGUGUCACGUTT -3’). [score:1]
Moreover, as a powerful inhibitor of EMT and cancer metastasis and progression, whether the epididymal miR-200 family contributes to the rarity of epididymal cancer is an intriguing question that requires further investigation. [score:1]
Then the set of putative miR-200 target genes was investigated whether they were significantly sat in the top or bottom of the ranked list. [score:1]
Based on these observations, the whole miR-200 family seemed to work as a group, which might achieve amplified biological effects. [score:1]
0124450.g006 Fig 6 (A) Two subfamilies of the miR-200 family with slightly different seed regions. [score:1]
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[+] score: 139
Other miRNAs from this paper: rno-mir-200a, rno-mir-200b
A preliminary study on mirnas induced by oxidative stress in HTM cells showed miR-200c as a highly up-regulated miRNA, and gene expression profile was analyzed after over -expressing miR-200c in HTM cells (data not published). [score:8]
Seven rats were injected with miR-200c mimic and scramble mimic (Dharmacon, 6 ug/10 ul) using The Max Suppressor In Vivo RNA-LANCER II (Bioo Scientific, Austin, TX) following manufacturer’s instructions; rats were injected twice, at days 2 and 6. Eight rats were injected with adenovirus expressing miR-200c inhibitor (miR-200c sponge, 1×10 [9] pfu, 10 µl) and with null adenovirus (empty virus, 1×10 [9] pfu, 10 µl). [score:7]
Gene expression profile was analyzed by gene arrays in HTM cells transfected with miR-200c or scramble control (data not showed); from a list of genes with fold change ≥2.0 or -2.0 and p-value ≤0.05 three genes ETAR, LPAR1 and FHOD1 (Table 2) were selected for further analysis because they were down regulated, predicted targets of miR-200c and affect cell contraction. [score:6]
The down-regulation of these genes was confirmed by Q-PCR in two different cell lines (HTM 36 and HTM 88), along with ZEB1 and ZEB2, two established targets of miR-200c and transcriptional repressors of E-cadherin and epithelial to mesenchimal transition [39]– [41] (Table 2). [score:6]
The effects of miR-200c on IOP were further supported by the increase in IOP observed after inhibition of miR-200c using an adenoviral vector expressing a molecular sponge. [score:5]
Quantitative –PCR (Q-PCR) and Affymetrix arrays values for some targets and predicted targets of miR-200c. [score:5]
Our results showed that cells transfected with miR-200c down-regulated ZEB1, ZEB2, FHOD1, LPAR1/EDG2, ETAR; the same treatment also down regulated RhoA at protein level. [score:5]
FHOD1 was recently described as a target of miR-200c; and here we identified ETAR, LPAR1/EDG2, and RhoA as novel targets of miR200c as well. [score:5]
To inhibit the activity of miR-200c a sponge was used, a miRNA sponge has complementary binding sites to a miRNA of interest that can sequester miRNAs from their endogenous targets and thus serve as a decoy [53]. [score:5]
Similarly, it is worth mentioning that microRNAs are known to have multiple targets, and it is likely that additional miR-200c targets might be involved in the observed effects of this miRNA on outflow facility. [score:5]
Some genes that significantly change expressions were selected for further analysis because they were predicted targets of miR-200c and affect cell contraction. [score:5]
Down-regulation of Etar, Lpar1 and RhoA proteins by miR-200c was confirmed by Western blot in HTM cells (Figure 1C and 1D). [score:4]
LPAR1, ETAR and RhoA are Direct Targets of miR-200c. [score:4]
MiRNA databases show that miR-200c shares complementarities with sequences in the 3′UTR of ETAR, LPAR1 and FHOD1 and these genes were found to be down-regulated by miR-200c in arrays and Q-PCR analyses. [score:4]
Recently, miR-200c has also been shown to suppress migration and invasion of cancer cells by interfering with the cytoskeletal organization through actin regulatory proteins, like FHOD1 and PPM1F, in a ZEB1/ZEB2 independent manner [43]. [score:4]
Consistent with the observed postranscriptional inhibition of multiple genes involved in the regulation of the contractile responses, HTM cells transfected with miR-200c showed a decreased response in cell traction forces. [score:4]
ETAR and LPAR1 are predicted as targets for miR-200c from three databases: Microcosm (http://www. [score:3]
LPAR1, ETAR and RhoA are new targets of miR-200c. [score:3]
Our previous studies have shown that miR-200c is highly expressed in TM cells [44]. [score:3]
FHOD 1 was recently described as a miR-200c target [43]. [score:3]
These factors were chosen because they are known to induce contraction of trabecular meshwork, and miR-200c targeted main receptors for ET-1 and LPA (ETAR and LPAR1), and a gene inducing stress fiber formation by thrombin activation (FHOD1). [score:3]
It also appeared to last longer than the short life of miR -mimics, suggesting that some of the changes induced by the increased miR-200c expression might persist for some time after miR-200c has returned to basal levels. [score:3]
MiR-200c Down-regulates Genes Involved in Cell Contraction. [score:3]
A potential regulator of the actomyosin system in TM cells is the miR-200 family. [score:2]
In conclusion, our results demonstrate for the first time the ability of a miRNA to regulate trabecular contraction and modulate IOP in vivo, making miR-200c worthwhile candidate for exploring ways to alter trabecular contractility with therapeutic purposes in glaucoma. [score:2]
Briefly, miR-200c sponge was obtained through amplifying the 3′UTR from the ZEB1 gene that contain two target sites for miR-200c, using the following primers: F-ggatccgcatttcagacatggacatgctattg and R-ctcgagattaatactgccaggtttgaagacatacag. [score:2]
MiR-200c Inhibits Contraction of TM cells in Collagen Populated Gels. [score:2]
Efficiency of transfection of mirnas in HTM cells was evaluated by the reduction of miR-200c established targets (Table 2) and by fluorescent microscopy and fluorescent activated cell sorting (FACSCAN) after transfection with a fluorescent mirna (Figure S1A, S1B and S1C). [score:1]
Panel A shows miR-200c pre-mirna sequences for Rattus novergicus (Rno-miR-200c; NCBI Reference seq: NR_031915.1) and Homo sapiens (hsa-miR-200c; NCBI Reference seq: NR_029779.1) and the miR-200c sequence used as mimic; the mature miRNA is highlighted in red. [score:1]
This effect was accumulative since it was higher after two injections of miR-200c mimic. [score:1]
In some instances miR-200c abolished almost completely the contractile response to these treatments (Figure 2C and 2D). [score:1]
The average difference between mean traction force in cells with and without serum in the control group was statistically significant; but in cells transfected with miR-200c there was no significant difference (Figure 3B and 3C). [score:1]
On average the cells in complete media showed the biggest difference in contraction between miR-200c and scramble (28.8 mm [2]). [score:1]
0051688.g001 Figure 1 (A) Predicted interactions between the seed region of miR-200c and the 3′UTRs from LPAR1, ETAR and RhoA. [score:1]
Furthermore, transfection of HTM cells with miR-200c significantly decreased traction forces in single cells in presence of serum. [score:1]
Further studies will be needed to fully understand the mechanism behind the effects of miR-200c in vivo. [score:1]
HTM18 miR200c S n = 14, SF n = 15; control S n = 16, control SF n = 10; HTM63 miR-200c S n = 12, SF n = 12; control S n = 14, control SF n = 15. [score:1]
HTM primary cells were transfected, at 50 to 70% confluency next day after plating, with hsa-miR-200c mimic, control mimic (scramble) or control fluorescent mimic DY547 (40 pmol) (Thermo Scientific, Chicago, IL) using lipofectamine 2000 (Invitrogen), following manufacturer’s instructions. [score:1]
The eyes injected with either miR-200c mimic or control showed a larger level of IOP fluctuations than those treated with adenoviral vectors, suggesting that the method of delivery could potentially influence IOP stability. [score:1]
0051688.g002 Figure 2 (A) Representative gels of HTM cells transfected with miR-200c or miR-control in complete media. [score:1]
The efficacy of miR-200c sponge was confirmed by Q-PCR in HTM cells (Figure S2B). [score:1]
Co-transfections in 293A cells with luciferase 3′UTR constructs (300 ng) and miR-200c mimic or scramble (20 pmol) was accomplished using Effectene (Qiagen). [score:1]
pAD-CMV-miR200c-sponge was transfected to 293A cells using lipofectamine 2000. [score:1]
Replication deficient adenoviruses for miR-200c sponge and null virus were prepared using the Getaway System from Invitrogen, following manufacturing’s instructions. [score:1]
Asterisk (**) represent significant at p<0.01 between miR-200c and control. [score:1]
0051688.g004 Figure 4(A) Mean IOP percent changes in rats injected with miR-200c mimic and control mimic (n = 7). [score:1]
Analysis of miR-200c Interaction with 3′UTRs. [score:1]
In complete media, cells transfected with miR-200c exhibited less mean traction force than cells with miRNA control; this difference was reduced when cells were kept in media without serum. [score:1]
MiR-200c mimic significantly reduced luciferase expression in cells co -transfected with the 3′UTR of ETAR, LPAR1 and RhoA compared to mimic control (scrambled) The decrease in luciferase activity was prevented when the 3′UTR complementary sequences were used (Figure 1B). [score:1]
Figure 2A showed the difference in contraction between cell transfected with control and miR-200c for each cell line. [score:1]
Figure S2 Alignment of human and rat miR-200c sequences and evidence of functionality of the miR-200c sponge. [score:1]
Panel C shows the mean difference in traction stresses between miR-200c S/SF and mimic control S/SF in HTM. [score:1]
The maximum difference between both eyes was observed at day 6 with average IOP of 14.7 mmHg in the control and 24.2 mmHg in miR-200c sponge, this effect was statistically significant during the 6 days that the effect lasted (Figure 4). [score:1]
The observed effects of miR-200c on the responses induced by ET-1, LPA and TGFβ2 suggest that miR-200c might exert important effects on IOP. [score:1]
Gene array analysis was conducted with either miR-200c mimic or mimic control on a HTM primary cell line (HTM23). [score:1]
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4
[+] score: 79
Other miRNAs from this paper: rno-mir-21, rno-mir-205
Because bioinformatic analysis has indicated that miRNAs frequently interact with transcription factors in feedback and feedforward loops to regulate their target genes [43, 44]; therefore, further experiments are required to elucidate the function and role of these potential target genes and the upregulated miR-21, as well as miR-200c and miR-205, in ischemic injury. [score:9]
In the experiment that we performed to identify the minimal ischemic time that would induce the expression of these 3 miRNAs, upregulation of miR-21 and miR-200c was noted after 4 h of reperfusion following 1 h and 2 h, but not 30 min of ischemia; in addition, upregulation of miR-205 was noted after 4 h of reperfusion following 2 h, but not 30 min or 1 h of ischemia (Figure 2). [score:9]
This study has profiled an increased expression of miR-21, miR-200c, and miR-205 in the gracilis muscle following ischemic injury and identified four potential target genes (Nqo1, Pdpn, CXCL3, and Rad23b) of the miR-21 by using different prediction algorithms and monitoring the expression of miRNA and mRNA at different time point on a genome-wide basis. [score:7]
Our data also showed that miR-200c and miR-205 were actively regulated after ischemia but their expression pattern changed after reperfusion, indicating their temporal expression during ischemic injury. [score:6]
However, as shown in the Figure 2, in the investigation of minimal ischemic time that would induce the expression of these 3 miRNAs, we had demonstrated that 1 h of ischemia was able to increase the expression of miR-21 and miR-200c and 2 h of ischemia would increase the expression of these three miRNAs, implying the epigenetic regulation could be induced by a shorter time of ischemia before a remarked pathophysiologic change could be observed by a longer time of ischemia. [score:6]
Ischemia for only 1 h was sufficient to induce the expression of miR-21 and miR-200c during the reperfusion stage; and 2 h of ischemia were required to induce the expression of miR-205. [score:5]
The miR-200c and miR-205 were not upregulated at all 4 indicated times. [score:4]
Those upregulated miRNAs (miR-21, miR-200c, and miR-205) that were identified from the miRNA array were quantified by real-time RT-PCR with the Applied Biosystems 7500 (Applied Biosystems, USA). [score:4]
Real-time RT-PCR demonstrated that, with 2-fold increase after 4 h of ischemia, a maximum 24-fold increase at 7 d, and a 7.5-fold increase at 14 d after reperfusion, only the miR-21, but not the miR-200c or miR-205 was upregulated throughout the experimental time. [score:4]
In this study, we demonstrated that 3 miRNAs (miR-21, miR-200c, and miR-205) were significantly upregulated in a different pattern in the gracilis muscles following ischemic injury. [score:4]
Figure 2 Expression of miR-21, miR-200c, and miR-205 detected with real-time RT-PCR in the gracilis muscles following indicated ischemic times (30 min, 1 h, and 2 h) and reperfusion for 4 h. Bars represent means ± standard deviation of 5 independent experiments; *, P < 0.05 vs. [score:3]
In the investigation of the differentially expressed miRNAs from the miRNA array experiments, there were only 3 miRNAs (miR-21, miR-200c, and miR-205) that showed an increased expression in the gracilis muscles after 4 h of ischemia and 4 h of reperfusion. [score:3]
Figure 1 Expression of miR-21, miR-200c, and miR-205 detected with real-time RT-PCR in the gracilis muscles following 4 h of ischemia and reperfusion for indicated times. [score:3]
We did not detect an increased expression of miR-200c 1 d after reperfusion. [score:3]
Three miRNAs (miR-21, miR-200c, and miR-205) of 350 tested rat miRNAs were found to have an increased expression in the miRNA array. [score:3]
The miR-200c expression was increased 3.2 fold and was detected 2 h after reperfusion following 4 h of ischemia. [score:3]
The expression of miR-200c reached its maximum level at 4 h and lasted for up to 8 h after ischemic injury. [score:3]
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5
[+] score: 55
It has been suggested that different cell lines regulate miR-200 expression through distinct epigenetic mechanisms [27]. [score:4]
Downregulation of miR-200 family members might underlie kidney cyst formation in Dicer mutant kidneys. [score:4]
Members of the miR-200 family were highly expressed in the kidney, lung, small intestine, and exocrine glands (Figure 2(a)). [score:3]
Members of the miR-200 family are commonly expressed in tubular tissues, and it is impossible to classify these tissues using only the miR-200 family. [score:3]
The expression of miR-200a, miR-200b, miR-200c, miR-192, miR-194, and miR-449a was validated with real-time RT-PCR in rat tissues in order to discriminate the kidney from other tissues with a tubular structure. [score:3]
In the present study, the expression of miR-200c was higher in the lacrimal gland and salivary gland than in other tubular tissues. [score:3]
As expected, members of the miR-200 family were highly expressed in exocrine glands and epithelial cells. [score:3]
The miR-200 family consists of five members (miR-200a, miR-200b, miR-200c, miR-141, and miR-429), which are clustered and expressed as the miR-200b-200a-429 cluster at chromosomal location 1p36 and the miR-200c-141 cluster at chromosomal location 12p13. [score:3]
Members of the miR-200 family were highly expressed in the proximal tubule. [score:3]
Members of the miR-200 family were expressed at high levels in each tissue with a tubular structure (Figures 3(a)– 3(c)). [score:3]
In human tissues, the results of the miRNA array analysis showed that miR-200a, miR-200b, and miR-200c (miR-200 family) were highly expressed in the kidney, lung, salivary gland, trachea, colon, prostate, liver, and pancreas (Figure 1). [score:3]
To examine the miR-200 family in the kidney, miRNA array analysis was performed to compare expression in the proximal tubule and mesangial cells. [score:3]
Our results showed that miR-200 family members were expressed at high levels in various tissues with a tubular structure: the kidney (proximal tubule and collecting duct), lung, pancreas (duct cells), small intestine (intestinal villus), bile duct, and exocrine glands (duct cells). [score:3]
The lacrimal gland and salivary gland are formed from the ectoderm, and the expression ratio of miR-200a/b and miR-200c might depend on the germ layer. [score:3]
Members of the miR-200 family are highly expressed in the kidney and lung. [score:3]
We assessed whether the plasma concentrations of miR-200a, miR-200b, and miR-200c could be used as a biomarker for acute kidney injury (Figure 4). [score:1]
miR-200c was not detected in urine. [score:1]
These results suggest that the miR-200 family is closely associated with tubular structure. [score:1]
In the future, we will assess the potential of the urinary miR-200 family as biomarkers of the renal tubular dysfunction in humans. [score:1]
Patel et al. have reported that miR-200 family members play important roles in renal tubule maturation by repressing Pkd1 in the kidney [25]. [score:1]
We assessed whether the urinary concentrations of miR-200a and miR-200c could be used as a biomarker for renal tubular dysfunction (Figure 5). [score:1]
We assessed whether the miR-200 family could be used as a biomarker for kidney injury. [score:1]
Consistently, the plasma concentrations of the miR-200 family members and miR-192 and miR-194 increased significantly. [score:1]
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6
[+] score: 54
Overexpression of the microRNA hsa-miR-200c leads to reduced expression of transcription factor 8 and increased expression of E-cadherin. [score:7]
In B13 cells, the absence of the expression of all members of the miR-200 family correlated with higher expression levels of Zeb1 and Zeb2 and reduced expression of both E-cad mRNA and protein levels compared to its parental cell line. [score:6]
The analysis of differentially expressed miRNAs between AR42J and B13 cells by using revealed specific expression of all the members of the miR-200 family (miR-200a, miR-200b, miR-200c, miR-141-3p, miR-141-5p and miR-429) in the parental cell line AR42J, whereas none of these miRNAs were detected in the B13 subclone. [score:5]
These cell lines presented a minimum of 59 miRNAs differentially expressed, and the plasticity of B13 cells could be explained, at least partially, by repression of the miRNA-200 family and E-cadherin as well as increased expression levels of Zeb1/Zeb2. [score:5]
miR-200 family members target and inhibit ZEB1 and ZEB2 factors which are key factors in epithelial-to-mesenchymal transition (EMT) [33– 35]. [score:5]
Also, overexpression of miR-200c leads to increased expression of E-cadherin, which maintains epithelial phenotypes in cells [33]. [score:5]
Moreover, miR-200 family members target and inhibit ZEB1 and ZEB2 factors, which blocks epithelial-mesenchymal transition (EMT) and causes cells to maintain an epithelial state [33– 35]. [score:5]
The expression levels of Zeb1 and Zeb2 were significantly higher in the B13 subclone compared to AR42J cells (2.7- and 57-fold, respectively) (Fig 5A and 5B), whereas expression of E-cad was 52-fold lower (Fig 5C), which agree with the expected biological activity of miR-200 family in each cell type. [score:4]
Notably, all members of the miR-200 family (miR-200a, miR-200b, miR-200c, miR-141-3p, miR-141-5p and miR-429), which has been shown to be enriched in differentiated tissues such as ectoderm and endoderm and is largely excluded from the mesoderm [30– 32], were specifically expressed in AR42J cells and absent in the B13 subclone. [score:3]
There is strong evidence demonstrating that expression of the miR-200 family is enriched in terminally differentiated cells, such as epithelial tissues, and that it is undetected in pluripotent cells, such as mesenchymal cells [30– 32]. [score:3]
Relative miRNA expression levels of miR-200c-3p (A), miR-141-3p (B), miR-325-3p (C), miR-2137 (D), miR-210-3p (E), miR-181a-5p (F), miR-204-5p (G), miR-455-3p (H), miR-137-3p (I), miR-135a-5p (J), miR-384-5p (K) in rat exocrine fractions, rat islets, AR42J cells, B13 cells and B13 transduced with Ad-GFP or Ad-PNM at 4 days post-transduction, quantified by individual qPCR assays. [score:2]
0145116.g006 Fig 6Relative miRNA expression levels of miR-200c-3p (A), miR-141-3p (B), miR-325-3p (C), miR-2137 (D), miR-210-3p (E), miR-181a-5p (F), miR-204-5p (G), miR-455-3p (H), miR-137-3p (I), miR-135a-5p (J), miR-384-5p (K) in rat exocrine fractions, rat islets, AR42J cells, B13 cells and B13 transduced with Ad-GFP or Ad-PNM at 4 days post-transduction, quantified by individual qPCR assays. [score:2]
The differential expression of miR-200c-3p, miR-141-3p and miR-325-3p between AR42J and non-transduced B13 cells (Table 1) was further confirmed by the individual qPCR assays (Fig 6A–6C). [score:2]
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7
[+] score: 51
In epithelial cells, miR-200 family microRNAs and E-cadherin maintain higher level expression by repressing ZEB1, ZEB2 and TGFβ; on the other hand, in mesenchymal cells and tumors, the up-regulation of ZEB factors is triggered by TGFβ and suppresses the transcription of miR-141/200c by binding to their putative common promoter region. [score:8]
In our primary dataset, ZEB1 and ZEB2 were both up-regulated in six out of our eight ccRCC samples and, their expression levels were highly anti-correlated with the miR-200 family in both tumor and normal samples. [score:6]
Recently, several other groups have reported a role for the miR-200 family in the Epithelial-Mesenchymal-transition (EMT) and in cancer cell migration, the latter by directly targeting the transcription factors ZEB1 and ZEB2, which regulate E-Cadherin, a mediator of cell-cell adhesion [84, 85]. [score:5]
It is clear that loss of mir-200c regulation contributes to an increase in VEGFA transcript while for the other three (tumor suppressor genes), the level of transcript decreases because of a gain in the level of the corresponding microRNA. [score:4]
As confirmation of these results, down-regulation of miR-141 and miR-200c and their function on ZEB2 in ccRCC has recently been reported [87]. [score:4]
In Figure 2 we plot microRNA and mRNA levels for miR-200c and its target VEGFA. [score:3]
Expression levels of miR-200c and VEGFA in the primary dataset showing anti-correlation in both ccRCC and matched normal kidney tissue. [score:3]
Note that the levels of miR-200c and its target VEGFA are not only anti-correlated overall, but are also anti-correlated separately in both ccRCC and normal tissue. [score:3]
For instance, loss of miR-149, miR-200c and mir-141 causes gain of function of oncogenes (KCNMA1, LOX), VEGFA and SEMA6A respectively and increased levels of miR-142-3p, miR-185, mir-34a, miR-224, miR-21 cause loss of function of tumor suppressors LRRC2, PTPN13, SFRP1, ERBB4, and (SLC12A1, TCF21) respectively. [score:3]
B-E. Agilent chip expression levels of miR-200c, miR-244, miR-34a and miR-21 versus the levels of mRNA that they regulate: VEGFA, ERBB4, SFRP1 and SLC12A1 respectively as measured by qRT-PCR for 12 validation set samples The dark circles represent the values in ccRCC and the light circles in normal kidney. [score:2]
As the p-values in Figure 4 indicate, we validate a strong anti-correlation signature between mRNA levels of (KCNMA1, LOX), VEGF, SEMA6A, (LRRC2, PTPN13), SFRP1, ERBB4, SLC12A1 and TCF21, and their identified regulators: miR-149, miR-200c, mir-141, miR-142-3p, miR-185, mir-34a, miR-224 and miR-21 respectively. [score:2]
In Figure 3B-E, we plot the qRT-PCR expression levels of ERBB4, SFRP1, SLC12A1 and VEGFA versus Agilent chip measured levels of their regulatory microRNA (miR-224, miR-34a, miR-21 and miR-200c) for the twelve samples of Figure 3A. [score:2]
We also noted that in our data, the anti-correlation between VEGFA and the miR-200 family was strongest in normal kidney tissue, suggesting that loss of this regulation may be an important factor providing a permissive environment for HIF transcriptional signaling. [score:2]
This plot suggests that loss of miR-200c function in ccRCC contributes to increase in VEGF levels. [score:1]
Five miR-200 family members contain very similar seed sequences - AAUACU for miR-200b/200c/429 and AACACU for miR-200a*/141 [84]. [score:1]
Another example is the miR-200 family which includes two microRNA clusters, one on Chromosome 1p36.3 (miR-200a*/200b/429) and another on Chromosome 12p13 (miR-200c/141). [score:1]
We also found strong anti-correlation between VEGFA and the miR-200 family of microRNA: miR-200a*, 200b, 200c and miR-141. [score:1]
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8
[+] score: 50
Other miRNAs from this paper: rno-mir-141, rno-mir-192, rno-mir-200a, rno-mir-200b, rno-mir-429
Thus, in the glomeruli, in parallel to the enhanced expression of TGF-β1, a known inducer of EMT in epithelial cells [35], [36], we found downregulation of miR-200 family members and upregulation of ZEB2 that are, respectively, essential to maintain the normal epithelial phenotype and the EMT-inducing transcriptional factor [18], [20], [36], [37]. [score:9]
The downregulation of the microRNA-200 family, in response to enhanced TGFβ 1 expression, results in the reduction of epithelial markers and enhancement in mesenchymal markers and in ZEB 2, an EMT mediator. [score:6]
The fetal-programmed adult rats showed pronounced structural glomerular disorders with an accentuated and advanced stage of fibrosis, which led us to state that the glomerular miR-200 family would be downregulated by TGF-β1 action inducing ZEB 2 expression that may subsequently cause glomerular EMT. [score:6]
Additionally, in the present study, we demonstrated a significant enhancement in the expression of mesenchymal protein markers, including fibronectin, collagen 1 [α]1 and collagen 1 [α]2. Corroborating the present findings, Xiong et al. (2012) also verified downregulation of the miR-200 family induced by TGF-β1 in kidney cell culture [38]. [score:6]
Members of the miR-200 family and miR-192 act as protectors of the normal epithelial phenotype and are markedly downregulated in TGF-β -induced EMT [16], [17]– [21]. [score:4]
0071310.g009 Figure 9 Expression levels of mir-192, mir-141, mir-200a, mir-200b, mir-200c and mir-429 estimated by TaqMan RT-qPCR in isolated glomeruli of 16-wk old LP rats. [score:3]
Expression Profile of the miR-200 Family and of miR-192 in Isolated Glomeruli. [score:3]
Expression of the miR-200 family and miR-192. [score:3]
The miR-200 family members target both ZEB1 and ZEB2 (39). [score:3]
Expression levels of mir-192, mir-141, mir-200a, mir-200b, mir-200c and mir-429 estimated by TaqMan RT-qPCR in isolated glomeruli of 16-wk old LP rats. [score:3]
As miRNAs have been suggested as playing a key role in a variety of kidney diseases, we investigated the expression of the miR-200 family and miR-192 in isolated glomeruli from LP compared to NP offspring. [score:2]
The miR-200 family is divided into two groups according to their sequence seed: group 1 (miR-141 and miR-200a) and group 2 (miR-200b, miR-200c and miR-429) (38). [score:1]
Each cDNA of miRNA-200 family (miR-200a, miR-200b, miR-200c, miR-141 and miR-429) and miR-192 was quantified by real-time quantitative PCR using ABI Prism 7900 Sequence Detection System (Life Technologies, USA). [score:1]
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9
[+] score: 45
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200a, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
This approach proved effective at identifying several mRNAs whose relative levels of expression were positively correlated with that of their targeting miRNA(s), a subset of which are represented in Fig 9. These studies were therefore extended by employing a knockdown strategy in which an immortalized mouse caput epididymal epithelial cell line (mECap) was co -transfected with a cherry red reporter and miRNA mimics of either miR-200c, miR-486 (shown to be significantly up-regulated in the caput and caudal regions, respectively), or a scrambled negative control (mirVana). [score:9]
These candidate miRNAs included representatives that exhibited regulated patterns of expression from each of the two primary classes detected, namely: those with highest expression in the caput (let-7c-5p, let-7b-5p, miR-375-3p, miR-9-5p, miR-467d-3p, and miR-200c-3p), or highest expression in the cauda (miR-410-3p, miR-486-5p, and miR470c-5p) epididymis. [score:8]
As shown in Fig 10 this strategy proved effective in eliciting a significant reduction in the expression of both Mapk14 (targeted by miR-200c) (Fig 10A) and Foxo1 (targeted by miR-486) (Fig 10B) mRNA. [score:7]
In order to verify the next generation sequence data, nine differentially expressed miRNAs were selected for targeted validation using qRT-PCR, including representatives with highest expression in the proximal (caput: let-7c-5p, let-7b-5p, miR-375-3p, miR-9-5p, miR-467d-3p, and miR-200c-3p) and distal (cauda: miR-410-3p, miR-486-5p, and miR470c-5p) epididymis. [score:7]
0135605.g008 Fig 8In order to verify the next generation sequence data, nine differentially expressed miRNAs were selected for targeted validation using qRT-PCR, including representatives with highest expression in the proximal (caput: let-7c-5p, let-7b-5p, miR-375-3p, miR-9-5p, miR-467d-3p, and miR-200c-3p) and distal (cauda: miR-410-3p, miR-486-5p, and miR470c-5p) epididymis. [score:7]
In this context, qPCR confirmed highly significant down-regulation of let-7c-5p, let-7b-5p, miR-375-3p, miR-467d-3p, and miR-200c-3p between the proximal and distal epididymal segments. [score:4]
miRNA mimics of miR-200c-3p, miR-486-5p and a scrambled negative control (mirVana) were transfected separately at a concentration 5 nM using lipofectamine 2000 along with a cherry red internal control (0.5 μg) in Opti-MEM (Life Technologies) as per manufacturer’s instructions. [score:1]
To confirm the functional significance of epididymal miRNAs, an immortalized mouse caput epididymal epithelial cell line (mECap) was co -transfected with a cherry red reporter and miRNA mimics of either (A) miR-200c, (B) miR-486, or a scrambled negative control (mirVana). [score:1]
0135605.g010 Fig 10To confirm the functional significance of epididymal miRNAs, an immortalized mouse caput epididymal epithelial cell line (mECap) was co -transfected with a cherry red reporter and miRNA mimics of either (A) miR-200c, (B) miR-486, or a scrambled negative control (mirVana). [score:1]
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10
[+] score: 45
HL-1 atrial cardiomyocytes transfected with miR-29 and miR-200 (Fig 8) significantly down-regulate Cacna1c, Hnc4 and Ryr2 expression, while Camk2a was significantly decreased with miR-200 but not miR-29 (Fig 8). [score:6]
We provide herein evidences that miR-29 and miR-200 over -expression also contributes to ion channel expression remo deling. [score:5]
Observe that miR-29 and miR-200 over -expression leads to significant decreased of Cacna1c, Hcn4, Ryr2 and Camk2a (except for miR-29a) expression. [score:5]
miR-29 over -expression in HL1 atrial cardiomyocyte deregulate Cacna1c, Hnc4 and Ryr2, influencing therefore both the calcium handling and pacemaker activity, whereas miR-200 regulated Cacna1c, Ryr2 and Camk2a, in addition to Scn5a as previously reported [64], impacting therefore also in calcium handling. [score:5]
qPCR of left atrial chambers demonstrated that miR-1, miR-26b, miR-29a, miR-30e, miR-106b, miR-133 and miR-200 are up-regulated in HTD rats as compared to controls (Fig 1), demonstrating a similar microRNA expression profile as in atrial-specific Pitx2 deficient mice [14, 16]. [score:5]
HL-1 cells (6 × 10 [5] cells per well) were transfected with plasmids containing expression constructs for Pitx2, Wnt8a (Addgene), Wnt11a (Addgene, Cambridge, MA, USA), premiR-29a, pre-miR-200 (Exiqon) or siRNA-Pitx2c, siRNA-Zfhx3, siRNA-Enpep, siRNA-Sod2 (Sigma, Aldrich, Munich, Germany) as previously described [14, 34]. [score:3]
Thus these data demonstrate that miR-29 and miR-200 impaired expression also contributes to develop pro-arrhythmogenic substrates. [score:3]
miR-29a and miR-200 expression in HL-1 atrial cardiomyocytes transfected cells. [score:3]
Whereas it is wi dely documented that redox signaling can compromise ion channel functioning and calcium homeostasis in cardiomyocytes [67], in our system we observed no influence of H [2]O [2] administration on the regulatory impact of Pitx2 in distinct ion channels such as Scn5a, Kcnj2 and Cacna1c as well as multiple Pitx2-regulated microRNAs such as miR-1, miR-26, miR-29 and miR-200, in which redox impairment impact is less documented [68]. [score:3]
We have previously demonstrated that Pitx2 modulates expression of miR-29 and miR-200, among other microRNAs [16] and furthermore we have demonstrated in this study that modulation of distinct ion channel is greatly influenced by H [2]0 [2] administration while microRNA signature is mostly dependent on Pitx2c but not H [2]0 [2] administration. [score:3]
Several lines of evidence have already reported the key regulatory role of miR-1 [60– 62], miR-26 [63], miR-106b [64], miR-133 [65– 66] and miR-200 [64] in arrhythmogenesis. [score:2]
Modulation of miR-29 and miR-200 alters cardiac action potential determinants. [score:1]
Importantly, miR-29 and miR-200 are not significantly impaired in SHR atrial chambers, suggesting that Wnt-microRNA might be a pivotal candidate establishing fundamental differences between HTD and HTN in atrial arrhythmogenesis susceptibility. [score:1]
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11
[+] score: 44
As shown in Table II, 21 (ASH versus C16) and 11 (AFL versus C12) differentially expressed miRNAs were identified through the SAM algorithm, where miR-129 and miR-199a-3p exhibited the highest degrees of upregulation and downregulation between the ASH and the respective control groups, and miR-200c and miR-93 exhibited the highest upregulation and downregulation between the AFL and the respective control group. [score:15]
Five upregulated and eight downregulated miRNAs were observed in the AFL group compared with the expression levels in the control group, where miR-200c and miR-93 exhibited the greatest upregulation and downregulation, respectively, of the miRNAs. [score:14]
Overexpression of miR-200c or miR-200b has been demonstrated to upregulate E-cadherin expression, which promotes cell adhesion and thus reduces the initiation of an invasive phenotype (30). [score:8]
Similarly, the specific miRNA profile of AFL consisted of five downregulated (miR-93, miR-451, miR-221, miR-17-5p and miR-146a) and three upregulated (miR-200c, miR-490 and miR-195) miRNAs, in comparison to the control group. [score:7]
[1 to 20 of 4 sentences]
12
[+] score: 43
Collectively, chronic alcohol consumption superimposed on overnutrition -mediated cardiac pathology can putatively induce the following signaling mechanisms: (1) inhibition of mTORC1 and attenuation of protective compensatory mechanisms; (2) inhibition of INS metabolic signaling via downregulation of INS receptor, IRS-1, GLUT4; (3) downregulation of growth inhibitory mir-200 family microRNAs and (4) upregulation of mir-212 (Figure 4). [score:16]
The mir-200c has emerged as a cell growth inhibitor and targets apoptosis inhibitor FAP-1 [97]. [score:7]
The mir-200c also regulates stem cell factors, and it has been proposed that targeting the ZEB1-miR-200 feedback loop can lead to a promising treatment for fatal tumors, such as pancreatic cancer [98]. [score:4]
Therefore, it is conceivable that the modest mir-200c upregulation in cardiac tissue from an overnutrition mo del reflects a compensatory mechanism to delicately balance mTORC1 signaling and to control hypertrophy. [score:4]
Therefore, downregulation of mir-200 family microRNAs by alcohol can potentially increase growth and S6K1 protein levels. [score:4]
In contrast, rno-mir-200c was expressed modestly in ZO cardiac tissue. [score:3]
The mir-200 family microRNAs are shown to function as inhibitors of growth in many cell types. [score:3]
For example, therapeutic delivery of mir-200c is shown to ameliorate renal tubulointerstitial fibrosis [147]. [score:1]
The rno-mir-200c is located on chromosome 4 and interestingly, QTLs associated with mir-200c include heart rate QTL (Figure 3). [score:1]
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13
[+] score: 38
In addition to the down-regulated miRNAs, we obtained 7 up-regulated miRNAs (miR-200b, miR-200b-3p, miR-200b-5p, miR-200c-3p, miR-378b, miR-184, and miR-349) and 114 correlated miRNA and mRNA regulatory pairs. [score:8]
Among these DEMs, miR-33, miR-33-5p, miR-33-3p, miR-144-3p and miR-99a-3p were down-regulated in NAFLD, whereas miR-200b, miR-200b-3p, miR-200b-5p, miR-200c-3p and miR-349 were up-regulated. [score:7]
Additionally, miRNA-mRNA regulatory network analysis indicated that five down-regulated genes (Abcg8, Cyp1a1, Tmem255a, Gstm6 and Lat) in NAFLD rats were common targets of miR-200b-3p, miR-200b-5p and miR-200c-3p. [score:7]
The data presented in other studies are consistent with our findings, suggesting that miR-200b-3p, miR-200b-5p, miR-200c-3p and their target genes might be crucial regulators in the pathogenesis of NAFLD. [score:4]
We observed that the intersection genes Abcg8, Cyp1a1 and Tmem255a were the targets of miR-349, miR-378b, miR-200b-3p, miR-200c-3p, miR-200b-5p and miR-184 (Fig.   6B). [score:3]
Researchers observed that expression of miR-200b and miR-200c increased in high-fat-diet -induced NAFLD rat livers and free-fatty-acid -treated HepG2 cells and human hepatocytes [34]. [score:3]
Interestingly, we also observed that the expression levels of miR-200b-3p, miR-200b-5p and miR-200c-3p were remarkably increased in NAFLD rat livers. [score:3]
Additionally, we observed that miR-200b-3p, miR-200b-5p and miR-200c-3p all interacted with Abcg8, Cyp1a1, Tmem255a, Gstm6 and Lat (Fig.   6C,D). [score:1]
MiR-200b belongs to the miR-200 family, which is organized into two groups based on a single nucleotide difference in their seed sequence (group A: miR-141 and -200a; group B: miR-200b, -200c and −429) [33]. [score:1]
However, there are no reports about the correlation of miR-200b-3p, miR-200b-5p and miR-200c-3p with NAFLD. [score:1]
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14
[+] score: 37
miR-200 family members, including the downregulated miR-200a, are predicted to target genes that regulate synaptic function, neurodevelopment and neuronal survival [50]. [score:8]
Main miR-200 family target genes in the uterus, Stat5b, Zeb1 and Zeb2, were downregulated by multigenerational stress in the F1 generation. [score:6]
Furthermore, ZEB1 serves as transcription factor to inhibit the miR-200 family, thus enhancing Stat5b expression [19]. [score:5]
Including the downregulated miR-200b, the miR-200 family may exert peripheral effects to control uterine quiescence and contractility during pregnancy and labour [18]. [score:4]
The qRT-PCR confirmed changes of the selected miRNAs (Figure  4B), decreased expression of miR-96, miR-141, miR-182, miR-183, miR-200a, miR-200b, miR-429 and miR-451 in F2-SSS compared to F0-S animals, whereas miR-23b and miR-200c showed increased expression levels. [score:4]
Furthermore, stress altered miRNA expression patterns in the brain and uterus of F2 mothers, including the miR-200 family, which regulates pathways related to brain plasticity and parturition, respectively. [score:4]
Target genes of the miR-200 family include three particular genes, Stat5b, Zeb1 and Zeb2, all involved in pregnancy maintenance [18]. [score:3]
In order to validate miRNAs, we performed quantitative real time PCR (qRT-PCR) analysis of these differentially regulated miRNAs (n = 3 per group for F0, F1 and F2 generations, three replicates per sample): miR-23b, miR-96, miR-141, miR-181a, miR-182, miR-183, miR-200a, miR-200b, miR-200c, miR429 and miR-451. [score:2]
Ancestral programming by stress particularly involved the miR-200 family. [score:1]
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15
[+] score: 26
rno-miR-675-5p 4.143757751 Premature senescence of cardiac progenitor cells, G1 arrest, reduced cell proliferation, colony formation, migration and invasion rno-miR-183-3p 3.74730108 Regulates claudin-1 expression rno-miR-299a-5p 3.626723224 Anti-apoptotic role rno-miR-200c-3p 3.593610443 Targets the VEGF-VEGFR2 pathway and angiogenesis rno-miR-665 3.511737089 Negatively targets anti-apoptotic BCL2L1 rno-miR-291a-5p 3.457928187 VSMC migration rno-miR-490-5p 2.373358 Tumour suppressor rno-miR-1 2.505729 Suppresses cell growth rno-miR-133b 2.192279 Inhibits cell proliferation and invasion rno-miR-30c-1-3p 2.70761 Suppresses PXR expression rno-miR-294 2.010496 Promotes proliferation and differentiation rno-miR-127-5p 2.780488 A regulator of MMP-13 and suppresses cell growth rno-miR-503 2.327383 Inhibits cell proliferation and invasion Table 2 Twenty down-regulated miRNAs. [score:26]
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16
[+] score: 26
Several other miRNAs are predicted to target Klf4, among them miR-200c, which has relatively low expression in the embryo and early postnatal gland but significantly increased in expression by P15. [score:7]
We demonstrate that either miR-200c or miR-29c can down-regulate the expression of Klf4. [score:6]
0125153.g009 Fig 9(A) Log2 plots of microarray and qPCR expression profiles for miRNAs and their predicted target genes: miR-214, and Xbp1; miR-29c, miR-200c and Klf4; and miR-30a, miR-200a, and Sox11. [score:5]
As development proceeds, the observed increases of miR-29c, miR-375, miR-148, and miR-200c may drive the observed decreased expression of Klf4 mRNA. [score:4]
It has been shown that Klf4 is targeted by miR-200c [57, 58], and luciferase assays confirmed this interaction in a parotid cell line (Fig 9B). [score:2]
miR-200c regulates FGFR -dependent epithelial proliferation via Vldlr during submandibular gland branching morphogenesis. [score:2]
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17
[+] score: 25
Other miRNAs from this paper: rno-mir-26b, rno-mir-200a, rno-mir-200b
Members of miR-200 family are responsible for suppressing the translation of two members of zinc-finger E-box binding homeobox family, ZEB1/ δEF1 and ZEB2/SIP1. [score:5]
Recent studies have linked up miR-200 members to ZEBs [31] and revealed that miR-200 family mainly regulates EMT through directly targeting ZEB1 and ZEB2 mRNA. [score:5]
It is supposed that all members of miR-200 family are able to directly target ZEB1 and ZEB2 [11, 12]. [score:4]
Downregulation of miR-200 family was found significantly on day 7 after obstruction and more obviously on day 14 in UUO rats, which is accountable for initiation of EMT in tubular epithelial cells during renal fibrosis [12, 32]. [score:4]
Recent studies indicate that all members of miR-200 family, especially miR-200a, are implicated in inhibition of mesenchymal transition in tubular epithelial cells, partially mediating through E-cadherin restoration at initiation of EMT [12]. [score:3]
The miR-200 family plays a vital role in inhibiting EMT induced by TGF- β1 in renal tubular epithelial cells. [score:3]
Emerging evidences revealed that miR-200 plays a vital role in maintaining epithelial phenotype. [score:1]
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18
[+] score: 24
We found that miR-142, miR-200c, miR-212, miR-325, miR-361, miR-376c, miR-429, and miR-494 overexpression could down-regulate the CRH mRNA level (p < 0.05; Figure 6A), and there was no difference between these miRNAs and the negative miRNA control (p > 0.05) in terms of cell viability (Supplementary Figure S2A). [score:6]
Compared with overexpression of the scramble miRNA, miR-142, miR-200c and miR-376c could down-regulate CRH protein in primary cultured hypothalamus neurons (p < 0.05; Figure 7A). [score:5]
The binding site (B) of miR-142, miR-200c and miR-376c on the 3′-untranslatedregions (3′ UTR) of CRH and their mutant plasmid. [score:3]
Besides, miR-142, miR-200c, miR-325, miR-361, miR-376c and miR-429 overexpression could decrease the level of CRHR1 mRNA simultaneously (p < 0.05; Figure 6B). [score:3]
CRH protein expression (A) in primary hypothalamus neurons transfected with miR-142, miR-200c, miR-325, miR-361, miR-376c and miR-429 agomir or the negative control. [score:3]
In the dual luciferase reporter system, miR-142 (0.55 ± 0.037) and miR-376c (0.6 ± 0.045) over -expression significantly reduced the fluorescein enzyme activity (p < 0.01), whereas miR-200c had no change (p > 0.05; Figures 7B,C). [score:3]
The luciferase activity (C) of the miR-142, miR-200c, miR-376c onto the 3′ UTR of CRH. [score:1]
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19
[+] score: 20
We identified 2 miRNAs (miR-195 and miR-200c) that were distinctively expressed in the rat lung, 8 miRNAs that were co-expressed in the lung and heart and 1 miRNA that was co-expressed in the lung and kidney. [score:7]
Statistical analysis using Significant Analysis of Microarray (SAM) and Tukey Honestly Significant Difference (HSD) revealed 2 miRNAs (miR-195 and miR-200c) expressed specifically in the lung and 9 miRNAs co-expressed in the lung and another organ. [score:5]
Two miRNAs (rno-miR-195 and rno-miR-200c) were identified as being expressed specifically in the rat lung. [score:3]
Among the 12 selected miRNAs, two were lung-specific (miR-195 and miR-200c), one was kidney-specific (miR-10a), and three were co-expressed in the lung and heart (miR-126, miR-143 and miR-145) as determined by HSD, OSI and two-fold criteria. [score:3]
There are 5 and 3 nucleotide differences between miR-200c, and miR-200a and miR-200b, respectively. [score:1]
For example, only one of the miRNAs we identified as lung-specific, miR-200c, has been reported by other groups [37]. [score:1]
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20
[+] score: 15
Previous studies have shown that in fibrotic renal tissues the expressions of both miR-200 family and E-cadherin are significantly downregulated and that exogenous miR-200 could reduce renal fibrosis [30, 31]. [score:6]
Gregory PA Bert AG Paterson EL Barry SC Tsykin A Farshid G The miR-200 family and miR-205 regulate epithelial to mesenchymal transition by targeting ZEB1 and SIP1Nat Cell Biol. [score:4]
Park SM Gaur AB Lengyel E Peter ME The miR-200 family determines the epithelial phenotype of cancer cells by targeting the E-cadherin repressors ZEB1 and ZEB2Genes Dev. [score:3]
Pre-transfection of the miR-200 family can reverse TGF-β1 -mediated EMT in tubular epithelial cells [30, 32, 33]. [score:1]
Mongrco PS Rustgi AK The role of the miR-200 family in epithelial—mesenchymal transitionCancer Bid Ther. [score:1]
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21
[+] score: 15
Other miRNAs from this paper: rno-mir-200a, rno-mir-200b
Liu et al. [32] reported that they selected mRNAs with a conserved seed sequence in their 3′-UTRs for miRNAs that were diversely expressed between tumor and normal kidney, and identified target mRNAs whose expression had an negative correlation with that of miR; they found that there was an obvious inverse correlation between the miR-200 family and VEGF. [score:7]
Figure 2The targeting relationship between miR-200b and VEGFA geneNote: (A) The VEGFA 3′-UTR loci for combining miR-200b; (B) The luciferase expression was detected 48 h after 293T cells were co -transfected with VEGFA-3′-UTR-WT plasmid + miR-200 mimics plasmid, VEGFA-3′-UTR-MUT + miR-200b/NC; ** P<0.05 was considered statistically significant. [score:4]
The miR-200 family, including miR-200b, is a cluster of miRNAs, which are highly associated with epithelial–mesenchymal transition (EMT), wherein miR-200b was thought to be a key negative regulator of tumor metastasis, invasion, and chemo-sensitivity [7]. [score:2]
Note: (A) The VEGFA 3′-UTR loci for combining miR-200b; (B) The luciferase expression was detected 48 h after 293T cells were co -transfected with VEGFA-3′-UTR-WT plasmid + miR-200 mimics plasmid, VEGFA-3′-UTR-MUT + miR-200b/NC; ** P<0.05 was considered statistically significant. [score:2]
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22
[+] score: 14
Other miRNAs from this paper: rno-mir-200a, rno-mir-200b
As an important regulatory factor, the miR-200 family has been identified as suppressors of CSC-like or EMT-like phenotypes and functions in various normal and cancer cells [22], [23], [24], [36]. [score:4]
In addition to extensive participation in inhibiting epithelial mesenchymal transition (EMT) in various cancer cells [21], the miR-200 family is also inversely associated with regulating CSC phenotypes of breast cancer [22], [23], pancreatic cancer [24] and ovarian cancer [25]. [score:4]
More strikingly, miR-200 family members have been reported to be directly regulated by p53, further highlighting their role in tumor progression [46]. [score:3]
Recently, it has been confirmed that the miR-200 family plays a key role in negatively regulating the EMT process [21]. [score:2]
The miR-200 family is a group of evolutionarily conserved miRNAs, comprising five members (miR-200a, -200b, -200c, -141 and -429). [score:1]
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23
[+] score: 13
Members of the miR-200 family are known to suppress the Zeb2 transcription factor, and its inhibition promotes MET [53]. [score:5]
A number of miRNAs that were found to be upregulated in rat PSCs, such as the miR-290-295 cluster and the miR-200 family miRNAs, are involved in pluripotency induction and maintenance in mice 21, 47. [score:4]
Among the miRNAs upregulated in rat PSCs, we also identified miR-205 and members of the miR-200 family (miR-200a, miR-200b, miR-200c, miR-141 and miR-429), which promote mesenchymal to epithelial transition (MET) in mouse cells, a key step in fibroblast reprogramming [47]. [score:4]
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24
[+] score: 12
The analysis based on their fold changes showed a significant (P < 0.05) upregulation of miR-200c-3p (predicted to regulate IL-13 and VEGF-alpha), miR203a-3p (predicted to regulate IL-24 and PRKC α), miR29-3p (predicted to regulate TNFRS1A), and miR-21-5p (predicted to regulate NFk-B activity), in ocular tissues of LPS+RvD1 -treated rats compared to the vehicle+LPS group (Figure 4). [score:7]
These were miR-21-5p that is predicted to regulate NFk-B activity; miR-200c-3p that is predicted to negatively regulate IL-13, LEPR, NTF3, PRKC α, RIPK2, and VEGFA indicating decreased of proinflammatory cytokines [29]; miR-203a-3p predicted to regulate IL-24 and PRKC α; miR-29b-3p predicted to negatively regulate HDAC4, IL-1RAP, Lif, PDGF α, PDGFc, VEGFA, and TNFRSF1. [score:5]
[1 to 20 of 2 sentences]
25
[+] score: 11
We conclude that miR-9, miR-137, miR-200c, miR-381, miR-455, miR-495, and miR-543 represent an FGF2 -dependent system of multiple miRNAs that target specific genes operating in pathways and processes related to the lens differentiation (via c-Maf, Med1/PBP, N-myc, and Nfat5), miRNA-regulated RNA processing (via Cpsf6 and Tnrc6b) and nuclear/chromatin -based processes (via Med1/PBP, As1l, and Kdm5b/Jarid1b/Plu1). [score:4]
We found that seven miRNAs, including miR-9, miR-137, miR-200c, miR-381, miR-455, miR-495, and miR-543, target at least two “early” genes examined (i. e., c-Maf, N-Myc, and Nfib). [score:3]
Both c-Maf and Med1/PBP are predicted to be regulated by similar miRNAs, including miR-137, miR-200c, and miR-495 (Figure 7). [score:2]
The most connected miRNA identified here through the 12 top-ranking transcripts, including miR-495, miR-200c, miR-543, miR-381, and miR-9 (Figure 6A), retained their high-connectivity positions as identified by independent analysis shown earlier in Figure 6A. [score:1]
Seven miRNAs, including miR-9, miR-137, miR-200c, miR-381, miR-455, miR-495, and miR-543, and connections to specific functional groups of genes are shown. [score:1]
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26
[+] score: 10
To replicate the findings obtained using TLDA array plate, we selected three miRNAs that were upregulated (mir-124, miR-218, miR-29a) and three, miRNAs that were downregulated (miR-146a, miR-200c, miR-155) based on their highest degree of significance by chronic CORT treatment and re-analyzed their expression individually by qPCR. [score:9]
We confirmed this finding by analyzing the six most significant CORT -induced altered miRNAs (miR-218, miR-124, miR-29a, miR-146a, miR-200c, miR-155) by qPCR. [score:1]
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27
[+] score: 10
Other miRNAs from this paper: hsa-mir-205, hsa-mir-200c, rno-mir-205
In our previous study, we found that the anthraquinone derivative SZ-685C significantly suppressed the proliferation of the MMQ rat pituitary adenoma cell line and induced apoptosis through the downregulation of miR-200c [21]. [score:6]
Chen C. H. Xiao W. W. Jiang X. B. Wang J. W. Mao Z. G. Lei N. Fan X. Song B. B. Liao C. X. Wang H. J. A novel marine drug, SZ-685C, induces apoptosis of MMQ pituitary tumor cells by downregulating miR-200c Curr. [score:4]
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28
[+] score: 8
Indeed, an analysis of TargetScan revealed that the lesion in l11Jus05 lies within a seed sequence for the microRNA miR200 [13], [14]. [score:3]
Further studies of this mutation will help us to determine how miR200 regulates Med13. [score:3]
MiR200 is required for the mesenchymal/epithelial transition during embryonic development and is involved in cancer metastasis [38], [39]. [score:1]
We report the first lesion in a miR200 seed sequence in the 3′ UTR of Med13 in the lethal line l11Jus05, which dies at E 8.5 with cardiovascular and neural tube defects [16]. [score:1]
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29
[+] score: 7
Although the miR-200 family of miRNAs are most traditionally thought of as tumor-suppressive miRNAs because of their ability to target epithelial-to-mesenchymal transition-promoting transcripts, it is clear that miRNAs have many different functions through the targeting of hundreds of mRNAs, and thus different functions can be dominant in different biological settings [11, 28, 29]. [score:7]
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30
[+] score: 7
The ZEB-miR-200 feedback loop has been demonstrated to link EMT activation and the maintenance of stemness by suppressing stemness-inhibiting miRNAs and acting as a promoter of mobile, migrating CSCs [59]. [score:5]
Mol Biol Cell 33 Bendoraite A Knouf EC Garg KS Parkin RK Kroh EM 2010 Regulation of miR-200 family microRNAs and ZEB transcription factors in ovarian cancer: evidence supporting a mesothelial-to-epithelial transition. [score:2]
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31
[+] score: 7
Similarly, analysis of miRNA profiles of hippocampal neurons during I/R injury revealed that hydrogen inhibits I/R -induced expression of the miR-200 family by reducing ROS production, which has led to suppression of cell death [94]. [score:7]
[1 to 20 of 1 sentences]
32
[+] score: 7
For liver cancer, one recent study reported that miR-21, miR-31, miR-122, miR-221, miR-222 were significantly up-regulated in HCC tissues, whereas miR-145, miR-146a, miR-200c, and miR-223 were found to be down-regulated [15]. [score:7]
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33
[+] score: 6
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-22, hsa-mir-28, hsa-mir-29b-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-145a, mmu-mir-150, mmu-mir-10b, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-217, hsa-mir-218-1, hsa-mir-223, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-150, hsa-mir-195, hsa-mir-206, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-22, mmu-mir-29c, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-331, mmu-mir-331, rno-mir-148b, mmu-mir-148b, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-28a, mmu-mir-200c, mmu-mir-218-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, mmu-mir-217, hsa-mir-29c, hsa-mir-200a, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-135b, hsa-mir-148b, hsa-mir-331, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-10a, rno-mir-10b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-22, rno-mir-28, rno-mir-29b-1, rno-mir-29c-1, rno-mir-124-3, rno-mir-124-1, rno-mir-124-2, rno-mir-133a, rno-mir-143, rno-mir-145, rno-mir-150, rno-mir-195, rno-mir-199a, rno-mir-200a, rno-mir-200b, rno-mir-206, rno-mir-217, rno-mir-223, dre-mir-7b, dre-mir-10a, dre-mir-10b-1, dre-mir-217, dre-mir-223, hsa-mir-429, mmu-mir-429, rno-mir-429, mmu-mir-365-2, rno-mir-365, dre-mir-429a, hsa-mir-329-1, hsa-mir-329-2, hsa-mir-451a, mmu-mir-451a, rno-mir-451, dre-mir-451, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-10b-2, dre-mir-16a, dre-mir-16b, dre-mir-16c, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-29b-1, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-145, dre-mir-150, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-let-7j, dre-mir-135b, rno-mir-1, rno-mir-133b, rno-mir-17-2, mmu-mir-1b, dre-mir-429b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-133c, mmu-mir-28c, mmu-mir-28b, hsa-mir-451b, mmu-mir-195b, mmu-mir-133c, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, rno-let-7g, rno-mir-29c-2, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
For example, Landgraf et al. [18] studied the mammalian miRNA expression atlas by sequencing 250 small RNA libraries representing 26 different human and rodent organ systems and cell types, and Wang et al. [21] used home-made miRNA microarrays to identify the rat lung-specific miRNAs, miR-195 and miR-200c. [score:3]
Wang et al. [21] investigated the tissue-specific expression of miRNAs in six rat tissues (lung, heart, brain, kidney, liver and spleen), and found that miR-195 and miR-200c were expressed specifically in the lung. [score:3]
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[+] score: 6
Only five miRNAs (mmu-miR-451, mmu-miR-223, mmu-miR-92a, mmu-miR-200c, and mmu-miR-873) were differentially expressed, implying that the majority of miRNA downregulation associated with obesity could be reversed by LFD treatment. [score:6]
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[+] score: 6
Previous studies have linked the miR-200 family with the epithelial phenotype [34], and Korpal et al. [35] identified miR-200a as a suppressor of epithelial-mesenchymal transition (EMT) through direct targeting of ZEB1 and ZEB2 genes. [score:6]
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[+] score: 6
Current studies on diabetic processes indicate that miRNA-216, miRNA-217, and miRNA-21 target PTEN [6], and the miRNA-200 family targets friend of GATA (FOG)2 [32] to activate the Akt/mTOR signaling pathway, thereby mediating DN occurrence and development. [score:6]
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[+] score: 6
Dysregulated miR-124 and miR-200 expression contribute to cholangiocyte proliferation in the cholestatic liver by targeting IL-6/STAT3 signalling. [score:6]
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38
[+] score: 5
The involvement of miRNAs, such as the miR-200 family members (miR-200a, miR-200b, miR-200c, miR-141, and miR-429), regulating EMT has been shown earlier; in addition, their dysregulated expression was described in several oncologic conditions [11, 12]. [score:5]
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[+] score: 5
Expression changes respect to control/sham 1 dpo 7 dpo Name Liu Present Liu Present rno-miR-130b 1.42 NE rno-miR-146a 1.72 INC S rno-miR-15b 1.15 DEC NS rno-miR-17 1.74 INC NS rno-miR-18a 2.71 NE 3.41 NE rno-miR-200c 4.12 NE rno-miR-206 3.26 NE rno-miR-20a 1.69 NC rno-miR-20b-5p 1.83 NE rno-miR-21 1.37 INC S rno-miR-214 2.01 INC NS rno-miR-219-5p −1.82 DEC S rno-miR-221 1.1 NE rno-miR-223 3.58 INC S 3.4 INC S rno-miR-24-2* 2.41 DEC NS rno-miR-290 3.66 INC NS 2.96 DEC S rno-miR-378 1.31 INC NS rno-miR-410 −1.21 NE rno-miR-466b 3.05 DEC S rno-miR-541 1.11 INC S rno-miR-874 2,8 NEData restricted to microRNAs with significant changes in expression (2-fold or greater) according to Liu et al. [6]. [score:5]
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[+] score: 5
As shown in Figure 5b, VEGFA were targeted by the greatest number of the differential miRNAs, among which miR-429, miR-200b and miR-200c also interacted with VEGFC; in contrast, VEGFB was targeted only by miR-18a, miR-326, miR-330 and miR-128. [score:5]
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[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-21, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-33a, hsa-mir-98, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-133a-1, mmu-mir-135a-1, mmu-mir-141, mmu-mir-194-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-203a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-200b, mmu-mir-300, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-141, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-21a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-343, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, mmu-mir-200c, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, mmu-mir-29b-2, mmu-mir-135a-2, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-326, hsa-mir-135b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-21, rno-mir-26b, rno-mir-27b, rno-mir-27a, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-33, rno-mir-98, rno-mir-126a, rno-mir-133a, rno-mir-135a, rno-mir-141, rno-mir-194-1, rno-mir-194-2, rno-mir-200a, rno-mir-200b, rno-mir-203a, rno-mir-211, rno-mir-218a-2, rno-mir-218a-1, rno-mir-300, hsa-mir-429, mmu-mir-429, rno-mir-429, hsa-mir-485, hsa-mir-511, hsa-mir-532, mmu-mir-532, rno-mir-133b, mmu-mir-485, rno-mir-485, hsa-mir-33b, mmu-mir-702, mmu-mir-343, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, hsa-mir-300, mmu-mir-511, rno-mir-466b-1, rno-mir-466b-2, rno-mir-532, rno-mir-511, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466b-8, hsa-mir-3120, rno-mir-203b, rno-mir-3557, rno-mir-218b, rno-mir-3569, rno-mir-133c, rno-mir-702, rno-mir-3120, hsa-mir-203b, mmu-mir-344i, rno-mir-344i, rno-mir-6316, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-3569, rno-let-7g, rno-mir-29c-2, rno-mir-29b-3, rno-mir-466b-3, rno-mir-466b-4, mmu-mir-203b
We used TargetScan and miRanda database queries to obtain miRNAs, which had higher targeting combined with N4bp2, namely, miR-200, miR-429, miR-29 and miR-30. [score:5]
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[+] score: 4
Punctual mutation or deletion in cluster miR-96/182/183 produces ear or retina disorders while loss of function of the miR-200 family leads to defects in the terminal differentiation of olfactory precursors (Choi et al., 2008; Kuhn et al., 2011; Lumayag et al., 2013). [score:2]
Members of the miRNA-200 family regulate olfactory neurogenesis. [score:2]
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[+] score: 4
Murakami et al. reported that 11 miRNAs including miR-34, miR-199a-5p, miR-199, miR-200, and let-7e were up-regulated in a CCl [4] -induced fibrosis mo del mouse [31]. [score:4]
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[+] score: 4
Recent studies reported that miR-141-3p, belonging to the miR-200 cluster, is overexpressed in IUGR as well as in preeclamptic placentas 42– 44. [score:3]
Output from various microRNA prediction tools has been revealed that two members of miR-200 family, miR-200a-3p and miR-141-3p have conserved binding sites on the 3′UTR of TTR mRNA. [score:1]
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[+] score: 3
A previous study demonstrates that signal transducers and activators of transcription 3 (STAT3)-coordinated Lin-28-let-7-HMGA2 and miR-200-ZEB1 circuits initiate and maintain oncostatin M -driven EMT 5. The interplay of these EMT activators, such as HMGA2 and ZEB1 6– 8, represses E-cadherin expression. [score:3]
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[+] score: 3
[12] We showed that the inhibition of the miR-200 family and/or miR-182 family in SHSY5Y cells increased global protein conjugation by the abovementioned ULMs, and in so doing made these cells more resistant to OGD -induced cell death. [score:3]
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[+] score: 3
OTA increases miR-132 and miR-200c expression in porcine renal proximal tubular cells [33]. [score:3]
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48
[+] score: 3
Other miRNAs from this paper: rno-mir-200a, rno-mir-200b
Progesterone-activated genomic pathways could limit the expression of contractile agonists (e. g. oxytocin), receptors (e. g. prostaglandin receptors), contraction -associated protein (e. g. gap junctions), or microRNAs (e. g. miR-200 family) within the myometrium, and in turn cause long-term modulation of the uterine contractile phenotype [5, 18– 20]. [score:3]
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[+] score: 2
A subsequent bioinformatic prediction suggested that 18 of these miRNAs play key roles during tooth development, including let-7f, miR-128, miR-200b and miR-200c [11]. [score:2]
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[+] score: 2
Name Primers U6F: 5′-GCTTCGGCAGCACATATACTAAAAT-3′ R: 5′-CGCTTCACGAATTTGCGTGTCAT-3′ rno-miR-500-3pGSP: 5′-GGAAGGCACCTGGGCAAG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-499-3pGSP: 5′-GGGGAACATCACAGCAAGTC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-214-3pGSP: 5′-GGGGACAGCAGGCACAGAC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-20b-5pGSP: 5′-GGGGCAAAGTGCTCATAGTG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-877GSP: 5′-GGGGAAGTAGAGGAGATGGC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-451-5pGSP: 5′-GGGGGAAACCGTTACCATTAC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-3577GSP: 5′-GGGTTCTGTCCCTCTTGGC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-370-3pGSP: 5′-AGCCTGCTGGGGTGGAA-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-181d-5pGSP: 5′-GGGGCATTCATTGTTGTCG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-23b-3pGSP: 5′-GGGATCACATTGCCAGGG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-191a-5pGSP: 5′-GGCAACGGAATCCCAAAAG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-200c-3pGSP: 5′-GGGGTAATACTGCCGGGTAA-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-328a-3pGSP: 5′-AACTCGCCCTCTCTGCCC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ nutrients-07-01333-t002_Table 2 Table 2 Primers of mRNA targets. [score:1]
Name Primers U6F: 5′-GCTTCGGCAGCACATATACTAAAAT-3′ R: 5′-CGCTTCACGAATTTGCGTGTCAT-3′ rno-miR-500-3pGSP: 5′-GGAAGGCACCTGGGCAAG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-499-3pGSP: 5′-GGGGAACATCACAGCAAGTC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-214-3pGSP: 5′-GGGGACAGCAGGCACAGAC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-20b-5pGSP: 5′-GGGGCAAAGTGCTCATAGTG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-877GSP: 5′-GGGGAAGTAGAGGAGATGGC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-451-5pGSP: 5′-GGGGGAAACCGTTACCATTAC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-3577GSP: 5′-GGGTTCTGTCCCTCTTGGC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-370-3pGSP: 5′-AGCCTGCTGGGGTGGAA-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-181d-5pGSP: 5′-GGGGCATTCATTGTTGTCG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-23b-3pGSP: 5′-GGGATCACATTGCCAGGG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-191a-5pGSP: 5′-GGCAACGGAATCCCAAAAG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-200c-3pGSP: 5′-GGGGTAATACTGCCGGGTAA-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-328a-3pGSP: 5′-AACTCGCCCTCTCTGCCC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ nutrients-07-01333-t002_Table 2 Table 2 Primers of mRNA targets. [score:1]
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[+] score: 2
Other miRNAs from this paper: hsa-let-7a-2, hsa-let-7c, hsa-let-7e, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-2, hsa-mir-100, hsa-mir-29b-2, mmu-let-7i, mmu-mir-99b, mmu-mir-125a, mmu-mir-130a, mmu-mir-142a, mmu-mir-144, mmu-mir-155, mmu-mir-183, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-148a, mmu-mir-143, hsa-mir-181c, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-298, mmu-mir-34b, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-130a, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-125a, mmu-mir-148a, mmu-mir-196a-1, mmu-let-7a-2, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-mir-15a, mmu-mir-16-1, mmu-mir-21a, mmu-mir-22, mmu-mir-23a, mmu-mir-24-2, rno-mir-148b, mmu-mir-148b, hsa-mir-200c, hsa-mir-155, mmu-mir-100, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181c, hsa-mir-34b, hsa-mir-99b, hsa-mir-374a, hsa-mir-148b, rno-let-7a-2, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7i, rno-mir-21, rno-mir-22, rno-mir-23a, rno-mir-24-2, rno-mir-29b-2, rno-mir-34b, rno-mir-99b, rno-mir-100, rno-mir-124-1, rno-mir-124-2, rno-mir-125a, rno-mir-130a, rno-mir-142, rno-mir-143, rno-mir-144, rno-mir-181c, rno-mir-183, rno-mir-199a, rno-mir-200b, rno-mir-181a-1, rno-mir-298, hsa-mir-193b, hsa-mir-497, hsa-mir-568, hsa-mir-572, hsa-mir-596, hsa-mir-612, rno-mir-664-1, rno-mir-664-2, rno-mir-497, mmu-mir-374b, mmu-mir-497a, mmu-mir-193b, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-568, hsa-mir-298, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, hsa-mir-664a, mmu-mir-664, rno-mir-568, hsa-mir-664b, mmu-mir-21b, mmu-mir-21c, rno-mir-155, mmu-mir-142b, mmu-mir-497b, rno-mir-148a, rno-mir-15a, rno-mir-193b
Cluster Mapped ESTs Mapped cDNAs mir-497~195 Human: CR737132, DB266639, DA2895925, BI752321, AA631714 Human: AK098506.1 Rat: CV105515 mir-144-451 Human: R28106 Mouse: AK158085.1 Rat: AW919398, BF2869095, AI008234 mir-99b~let-7e~mir-125a Human: DB340912 Human: AK125996 mir-143~145 Human: BM702257 mir-181a-1~181b-1 Human: DA528985, BX355821 Mouse: BE332980, CA874578 mir-29b-2~29c Human: BF089238 Mouse: AK081202, BC058715 mir-298~296 Human: W37080 mir-183~96~182 Human: CV424506 mir-181c~181d Human: AI801869, CB961518, CB991710, BU729805, CB996698, BM702754 Mouse: CJ191375 mir-100~let-7a-2 Human: DA545600, DA579531, DA474693, DA558986, DA600978 Human: AK091713 Mouse: BB657503, BM936455 Rat: BF412891, BF412890, BF412889, BF412895 Mouse: AK084170 mir-374b~421 Human: DA706043, DA721080 Human: AK125301 Rat: BF559199, BI274699 Mouse: BC027389, AK035525, BC076616, AK085125 mir-34b~34c Human: BC021736 mir-15a-16-1 Human: BG612167, BU932403, BG613187, BG500819 Human: BC022349, BC022282, BC070292, BC026275, BC055417, AF264787 Mouse: AI789372, BY718835 Mouse: AK134888, AF380423, AF380425, AK080165 mir-193b~365-1 Human: BX108536 hsa-mir-200c~141 Human: AI969882, AI695443, AA863395, BM855863.1, AA863389 mir-374a~545 Human: DA685273, AL698517, DA246751, DA755860, CF994086, DA932670, DA182706 Human: AK057701 Figure 2 Predicted pri-miRNAs, their lengths, and features that support the pri-miRNA prediction. [score:1]
Cluster Mapped ESTs Mapped cDNAs mir-497~195 Human: CR737132, DB266639, DA2895925, BI752321, AA631714 Human: AK098506.1 Rat: CV105515 mir-144-451 Human: R28106 Mouse: AK158085.1 Rat: AW919398, BF2869095, AI008234 mir-99b~let-7e~mir-125a Human: DB340912 Human: AK125996 mir-143~145 Human: BM702257 mir-181a-1~181b-1 Human: DA528985, BX355821 Mouse: BE332980, CA874578 mir-29b-2~29c Human: BF089238 Mouse: AK081202, BC058715 mir-298~296 Human: W37080 mir-183~96~182 Human: CV424506 mir-181c~181d Human: AI801869, CB961518, CB991710, BU729805, CB996698, BM702754 Mouse: CJ191375 mir-100~let-7a-2 Human: DA545600, DA579531, DA474693, DA558986, DA600978 Human: AK091713 Mouse: BB657503, BM936455 Rat: BF412891, BF412890, BF412889, BF412895 Mouse: AK084170 mir-374b~421 Human: DA706043, DA721080 Human: AK125301 Rat: BF559199, BI274699 Mouse: BC027389, AK035525, BC076616, AK085125 mir-34b~34c Human: BC021736 mir-15a-16-1 Human: BG612167, BU932403, BG613187, BG500819 Human: BC022349, BC022282, BC070292, BC026275, BC055417, AF264787 Mouse: AI789372, BY718835 Mouse: AK134888, AF380423, AF380425, AK080165 mir-193b~365-1 Human: BX108536 hsa-mir-200c~141 Human: AI969882, AI695443, AA863395, BM855863.1, AA863389 mir-374a~545 Human: DA685273, AL698517, DA246751, DA755860, CF994086, DA932670, DA182706 Human: AK057701 Figure 2 Predicted pri-miRNAs, their lengths, and features that support the pri-miRNA prediction. [score:1]
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In zebrafish the miRNAs are detected in the eye, nasal epithelium, and sensory hair cells of the ear and neuromasts [26], and injection of miR-183 and miR-200 family members into zebrafish embryos have been demonstrated to impact development and affect neuromast migration [28]. [score:2]
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Other miRNAs from this paper: rno-mir-127, rno-mir-200a, rno-mir-200b, rno-mir-210
Other components of cell-cell adhesion structures such as E-cadherin are also regulated by miRNAs, in particular, miR-200 family. [score:2]
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A number of miRNAs have been shown to be relevant to fibrotic processes in diabetic nephropathy, including miR-29 and miR-200 families, miR-192 and miR-21 [14– 17]. [score:1]
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miR-429, miR-141 and miR-200a belong to the same miR-200 family. [score:1]
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For example, seven microRNAs, including miR-1, miR-200c, miR-340, miR-342, miR-325, miR-139 and miR-500 contributed to the association with heart failure (P-value = 2.74e-3). [score:1]
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We selected the top 9 miRNAs (miR-200a, miR-200b, miR-182, miR-429, miR-183, miR-200c, miR-141, miR-96 and miR-24) showing the highest standard deviations. [score:1]
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[+] score: 1
Other miRNAs from this paper: rno-mir-200a, rno-mir-200b
The miRNA-200 family was reported to be an important one in liver fibrogenesis 19 20. [score:1]
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On the other hand, other miRNAs such as, let-7i, miR-143, miR-148b-3p, miR-15b, miR-17-5p, miR-24, miR-27b, miR-92a, miR-106b, miR-125b-5p, miR-181a, miR-181c, miR-181d, miR-200c, miR-375, miR-107, miR-141, and miR-370, were present at higher levels in colostrum whey than in mature milk whey (Fig. 6). [score:1]
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Accumulated evidence revealed that Keap1 was controlled by microRNAs, such as miR-200, miR-141 and miR-28 [16]. [score:1]
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The roles of miR-200 family in EMT and fibrogenesis have been well defined by previous research [43, 44]. [score:1]
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They were miR-1, miR-21, miR-195 and miR-200c. [score:1]
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Other miRNAs from this paper: rno-mir-200a, rno-mir-200b, rno-mir-429
In tumours the transcriptional repressor ZEB1 has been found to repress miRs 200a 200b and 429 [[19], [20]] that are thought to function to maintain epithelial differentiation, and ZEB1 and miR200 are interconnected via a double negative feedback loop [21]. [score:1]
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The presence of miR-200 within the 3′-UTR of the human IDS gene was of special interest due to this miR family being induced and having a specific role during the late stages of neuronal differentiation (Beclin et al. 2016). [score:1]
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