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31 publications mentioning rno-mir-141

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-141. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 140
To test whether gain in regulatory microRNAs in undifferentiated BeWo cells, where the expression of the microRNAs is relatively low, lead to change in TTR expression, mature miR-200a-3p or miR-141-3p mimics were transfected into BeWo cells in the absence or presence of the respective inhibitors. [score:8]
Figure 4Overexpression and inhibition of miR-200a-3p and miR-141-3p regulate TTR and its function in human trophoblast cells. [score:6]
In summary, we identified TTR as a direct target of miR-141-3p or miR-200a-3p and demonstrated that TTR and these microRNAs are reciprocally expressed during human trophoblast differentiation. [score:6]
Successful reversal of this suppression phenomenon was observed with the addition of inhibitors for miR-200a-3p and miR-141-3p along with the respective mimics (Fig.   2b and d). [score:5]
Significant up-regulation of both miR-141-3p and miR-200a-3p levels was observed along with TTR down regulation in differentiating human trophoblast cells. [score:5]
Over expression of either miR-200a-3p or miR-141-3p using mimics in undifferentiated BeWo cells led to reduced expression of TTR transcript. [score:5]
Our data revealed that overexpression of miR-200a-3p or miR-141-3p repressed the expression of TTR in human trophoblast cells. [score:5]
These data are rather intriguing since miR-141-3p emerges as a central regulator of various genes pivotal for proper embryonic development and can be used as a potential biomarker as well as therapeutic target to combat IUGR. [score:5]
Upregulation of this microRNA was also found in placental tissue from FGR patients where miR-141 was found to down regulate E2F3 and PLAG1 [44]. [score:5]
Figure 2MiR-200a-3p and miR-141-3p directly target TTR 3′-UTR. [score:4]
Ospina-Prieto S MicroRNA-141 is upregulated in preeclamptic placentae and regulates trophoblast invasion and intercellular communicationTransl. [score:4]
In agreement with these data, miR-141-3p was found to be up-regulated in labyrinth zone of IUGR rat placenta. [score:4]
Tang Q miR-141 contributes to fetal growth restriction by regulating PLAG1 expressionPLoS ONE. [score:4]
Our finding that miR-141-3p and miR-200a-3p are involved in the regulation of TTR during trophoblast differentiation provides yet another mechanism by which microRNA adds a complementary layer of control at the post-transcriptional level to developmentally indispensible genes known to be transcriptionally regulated. [score:4]
These data strongly suggest that miR-200a-3p and miR-141-3p may regulate the expression of TTR and consequently TTR -mediated delivery of thyroxin hormone in placental trophoblast cells. [score:4]
The putative binding sites for miR-141-3p and miR-200a-3p on 3′-UTRs of human and rat TTR were identified using the TargetScan mouse 6.0, PicTar, microRNA. [score:3]
In line with our previous results, down regulation of TTR mRNA and protein upon differentiation was associated with significant up regulation of both miR200a-3p and miR-141-3p (Fig.   3f). [score:3]
Similarly microRNA inhibitors for miR-141-3p or miR-200a-3p (Ambion, USA) were transfected at a final concentration of 200 nM to prove the specificity of the microRNA action. [score:3]
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]
To validate whether TTR mRNA is a direct target of miR-200a-3p and miR-141-3p, dual luciferase reporter assay was performed in HEK293 cells. [score:3]
Our study on conserved microRNAs as plausible regulators of TTR biogenesis led to identification of two microRNAs, miR-200a-3p and miR-141-3p that directly bind to the 3′-UTR of TTR. [score:3]
Figure 3Differentiation of human trophoblast cells (BeWo) is associated with reciprocal expression of hTTR and miR-200a-3p, miR-141-3p. [score:3]
It was further demonstrated by our group that miR-141-3p regulates IGF2 during mouse placental development [48]. [score:3]
MiR-141-3p is highly expressed with concurrent down regulation of TTR in human IUGR fetal placenta. [score:3]
Since TTR biogenesis by placental trophoblast cells is crucial for proper fetal development, our results on miR-141-3p and miR-200a-3p in regulating T [4] uptake by human trophoblast cells led to next set of experiments using IUGR rat mo del as well as in human IUGR placentas. [score:3]
Recent reports have shown that, miR-141 is secreted from placental trophoblast and is up regulated in the third trimester (29–40 weeks) of pregnancy, but its expression is increased abnormally in preeclamptic placentas when compared with normal placentas 42, 43. [score:3]
Saha S Choudhury J Ain R MicroRNA-141-3p and miR-200a-3p regulate insulin-like growth factor 2 during mouse placental developmentMol. [score:3]
These data indicate that miR141-3p and miR-200a-3p might play important roles in regulating TTR during normal placental development. [score:3]
In brief, BeWo cells were transfected with miR-141-3p or miR-200a-3p mimic alone or mimic plus inhibitors as described above. [score:3]
Figure 5Induction of IUGR during pregnancy in rats impacts TTR and the regulatory microRNAs, miR-200a-3p and miR-141-3p. [score:2]
Mutated version of hTTR 3′UTR (5′-CGGTGCT-3′) were generated by introducing two point mutations in the seed region (5′-CAGTGTT-3′) of miR-141-3p and miR-200a-3p. [score:2]
Interestingly, our data highlight that in human IUGR placenta the regulation of TTR by miR-141-3p and not miR-200a-3p is physiologically relevant like that in rat. [score:2]
MiR-141-3p or miR-200a-3p can regulate endogenous TTR protein levels as well as thyroxin uptake by human trophoblast cells. [score:2]
Cells were transfected with microRNA mimics for miR-141-3p or miR-200a-3p (Ambion, USA) individually at a final concentration of 200 nM (titrated for maximum down regulation of TTR prior to this experiment, data not shown) using Lipofectamine RNAiMAX (Invitrogen, USA) as per manufacturer’s instructions. [score:2]
On the contrary, under pathophysiological conditions, such as, IUGR, only miR-141-3p is relevant and it regulates TTR levels both in rats and human during IUGR. [score:2]
This data clearly indicates that both miR-200a-3p and miR-141-3p have the ability to regulate endogenous TTR protein levels in human trophoblast cells. [score:2]
Leading on from this, we tested the role of miR-141-3p and miR-200a-3p in term placenta from human control and IUGR pregnancies. [score:1]
Figure 1Cellular source of TTR in developing rat placenta and miR-200a-3p, miR-141-3p binding sites on 3′-UTR of TTR mRNA (a) Quantitative real time PCR analysis of TTR mRNA from rat placental samples at different days of gestation. [score:1]
Both miR-141-3p and miR-200a-3p share a common microRNA response element (MRE) on the 3′UTR of TTR transcript, which is highly conserved across species including humans (Fig.   1c). [score:1]
As expected, miR-141-3p was significantly up regulated in the labyrinth zone of the IUGR placentae as compared to control. [score:1]
Using various bioinformatic software, binding sites of two microRNAs, miR-141-3p and miR-200a-3p were identified to be present in the 3′-UTR of human TTR and were found to be conserved across species. [score:1]
These trophoblast cells can be used as an ex vivo mo del system for studying the effects of miR-141-3p and miR-200a-3p on endogenous TTR during trophoblast differentiation. [score:1]
In the first construct 14–263 nucleotide of 3′UTR of TTR containing the putative MRE for miR-200a-3p and miR-141-3p (5′-CAGTGTT-3′) was cloned downstream of the firefly luciferease reporter in the pmirGLO plasmid and was denoted as ‘wild type’. [score:1]
They also have shown that in IUGR patients, elevated concentration of miR-141-3p can repress PLAG1 at both transcriptional and posttranscriptional levels. [score:1]
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]
These results along with our data indicate that miR-141-3p might function differently in different cellular and physiological context. [score:1]
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[+] score: 58
Expression of miR-129, miR-130a, miR-130b, miR-141, miR-218b and miR-3588 were uniquely suppressed in mid dose but then elevated in high dose, with opposite expression to their target genes. [score:9]
However, since OTA treatment induces miRNA-141, a regulator of Keap1[37], in 2 and 26 weeks after OTA adminstration, it seems impossible that an elevation in the expression of Keap1 is due to down-regulation of miRNA-141. [score:7]
In agreement with sequencing data, miR-129, miR-130b and miR-141 were down-regulated in CM and up-regulated in CH, although no signicance was found in miR-141. [score:7]
The expression of target genes of miR-129, miR-218b, miR-141,miR-130a, miR-130b, miR-3588 at 13 weeks. [score:5]
Both of miR-130b and miR-141 were up-regulated after administrated with OTA for 4 weeks (Figure  10a). [score:4]
No relevant pathways and GOBPs were found to be regulated by miR-141 and miR-3588, which might be explained by the less putative targets prediction of the two miRNAs. [score:4]
Sepp1, a target of miR-141, is a major extracellular selenoprotein that is synthesized and secreted from the kidneys and plays critical roles in body selenium homeostasis. [score:3]
Among these 77 miRNAs, those with ≥ 2-fold down-regulation in CM compared to CK (miR-129, miR-130a, miR-130b, miR-141, miR-218b and miR-3588) were selected for bioinformatic analysis. [score:3]
The mRNA expression of Smoc2/Dcn (miR-129), Emp1/Rapgef5 (miR-218b), lgfbp3/sepp1 (miR-141), lgfbp3/Sepp1/Col1a2/Edem1 (miR-130a/miR-130b) and Edem1/Dpt (miR-3588) at 13 weeks are strongly correlated with its corresponding miRNAs shown in the parentheses. [score:3]
The expression of miR-129, miR-130a, miR-130b and miR-141 was also examined in kidneys of rats in groups of 4 weeks and 26 weeks. [score:3]
In the 26-week group, the expression of miR-129 and miR-130b were decreased, while miR-141 was increased (Figure  10c). [score:3]
Figure 10 analysis of miR-129, miR-130a, miR-130b and miR-141 expression in the kidneys of the rats in 4 weeks (BK, BM and BHgroups, Figure 10 a), 13 weeks (CK, CM and CH groups, Figure 10 b) and 26 weeks (DK, DM and DH groups, Figure 10 c). [score:3]
KEGG and GO enrichment analyses were further performed in the six differentially expressed miRNAs (miR-129, miR-130a, miR-130b, miR-141, miR-218b and miR-3588), demonstrating that “phosphatidylinositol signaling system”, “pancreatic cancer” and “MAPK signaling pathway” were mostly significantly enriched. [score:3]
Moreover, miR-141 is valuable in disscussion part) were analyzed by to validate the results of high throughput sequencing data. [score:1]
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[+] score: 56
SEMA6A was confirmed as a direct target of miR-141 by over -expressing miR-141 in a ccRCC cell line and showing strong down-regulation of the SEMA6A transcript. [score:9]
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]
Our hypothesis (prediction) from these various observations is that in normal kidney, the expression level of HIF2α and its downstream targets (VEGFA, TGFβ etc) are regulated by miR-141, 200a*, 200b and 200c and the loss of this microRNA regulation, in concert with VHL loss, is responsible for activation of the HIF pathway. [score:7]
Finally, to establish that this method can accurately predict functional and direct microRNA/mRNA regulation, we performed an in vitro analysis of one microRNA (miR-141), and its identified direct target SEMA6A. [score:6]
The results (Figure 5) showed that introduction of pre-miR-141 produced a significant reduction in the level of SEMA6A mRNA, validating SEMA6A as a functional and direct target of miR-141. [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 vitro validation of SEMA6A as a target of miR-141. [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]
Figure 5 Validation of a Direct interaction between miR-141 and SEMA6A. [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]
One intriguing association which we have identified (miR-141 regulation of SEMA6A) is highly significant for therapy in ccRCC. [score:2]
We also found strong anti-correlation between VEGFA and the miR-200 family of microRNA: miR-200a*, 200b, 200c and miR-141. [score:1]
of in-vitro experiment on RCC cell line CRL-1611 transfected either with pre-miR-141 or a control pre-miR using either Fugene (Fu) or Hyfect (Hy). [score:1]
Hence, our results imply that miR-141 may have a role in gene therapy. [score:1]
The regulation of SEMA6A by miR-141 was verified by a transfection assay. [score:1]
Human renal cell adenocarcinoma cells (ATCC, CRL-1611) were transfected with either the negative control pre-miR or hsa-miR-141 (Ambion) using either FuGENE HD (Roche) or HyFect (Denville scientific) transfection reagents. [score:1]
There is clear reduction in mRNA of SEMA6A upon introduction of miR-141 by either transfection method in these cells. [score:1]
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[+] score: 24
In contrast, miR-200a-3p expression, and potentially the expression of all miRNAs specified by the three clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429, tend to be up-regulated with similar FCEs in both experimental conditions. [score:8]
Co-variation of miRNA expression also demonstrated that the transcription and maturation of clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429 are co-regulated in ARC. [score:4]
Altogether our new and previous findings point to a trend to the long-term overexpression of clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429 in the ARC of adult rats and mice having experienced low levels of leptin/leptin signaling during the perinatal period. [score:3]
Ten miRNAs are produced by clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429. [score:1]
Among those miRNAs were all the 10 miRNAs produced from miR gene clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429. [score:1]
miRNAs specified by clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429 have been identified as miRNAs of functional importance in sensory organs. [score:1]
miRNA-3ps specified by the three clusters displayed extensive sequence identity all along although the seed region of miR-141-3p and −200a-3p differs by one nucleotide at position 4 with that of miR-200b-3p, −200c-3p, and −429-3p. [score:1]
Among the 15 (3.6%) miRNAs displaying MAX/MINs larger than this value, 8 were produced from three miR gene clusters, namely the miR-96/182/183 cluster and the two evolutionary-related clusters miR-141/200c and miR-200a/200b/429 (Table 2). [score:1]
The specific case of clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429. [score:1]
In these groups, miRNAs produced from clusters miR-96/182/183, miR-141/200c, miR-200a/200b/429 also appeared as hypervariable miRNAs (see Table 2). [score:1]
Figure 5 The specific case of the miRNAs specified by clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429. [score:1]
miRNAs miR-200a-3p and miR-141-3p displayed MAX/MINs higher than the value of 8.3 in groups HF-C and/or HF-HF. [score:1]
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[+] score: 23
Of the 123 miRNAs, 15 were differentially expressed in the AS and CS mo del groups, of these, four were significantly upregulated (rno-miR-296, rno-miR-141, rno-miR-382 and rno-miR-219-5p; Table IV) and 11 were downregulated (significantly downregulated, rno-miR-135a and rno-miR-466b; Table V). [score:12]
Of these 15 miRNAs, rno-miR-296, rno-miR-141, rno-miR-382 and rno-miR-219-5p were significantly upregulated, particularly miR-296 (Table IV), and 11 were downregulated (miR-135a and miR-466b were significantly downregulated, particularly miR-135a; Table V). [score:10]
In conclusion, rno-miR-296, rno-miR-141, rno-miR-382, rno-miR-219-5p, miR-135a and miR-466b may be involved in stress at the molecular level, thus causing myocardial injury. [score:1]
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[+] score: 20
To determine if the selected miRNA signature would predict significant changes in expression of genes within the canonical neoplastic and metastasis pathways, IPA was used to identify 1 upstream negative regulator (KRAS) of miR-141-3p and 6 downstream, positively regulated targets (AGO2, BCL2L11, AKT1, ZEB2, CDKN1B, BCL2) of the 4 miRNAs. [score:7]
IPA identified 4 focus miRNAs related to metastasis and upper gastrointestinal tract cancer (≥4 fold change) that were downregulated in metastasis positive samples versus metastasis negative samples: 1) miR-92a-3p (p = 0.0001, fold change >14), miR-141-3p (p = 0.0022, fold change >9), miR-451-1a (p = 0.0181, fold change >12) and miR133a-3p (p = 0.0304, fold change >9) (S2 Fig. ). [score:4]
miRNome analysis identified four down-regulated miRNAs in metastasis positive primary tumors compared to metastasis negative tumors: miR-92a-3p (p=0.0001), miR-141-3p (p=0.0022), miR-451-1a (p=0.0181) and miR133a-3p (p=0.0304). [score:3]
The upstream target KRAS has been shown to activate Zeb1, a repressor of miR-141-3p[35]. [score:3]
The 4 miRNAs (miR-92a-3p, miR-451a, miR-141-3p, and miR-133-3p) were significantly down regulated in metastasis positive tumors. [score:2]
The 4 focus miRNAs symbols miR-92a-3p, miR-141-3p, miR-451-1a, and miR133a-3p were mapped from the dataset ID rno-miR-32-5p, rno-miR-141-3p, rno-miR-451-5p, and rno-miR-133b-3p respectively. [score:1]
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[+] score: 15
Other miRNAs from this paper: rno-mir-192, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-429
The current study has shown that LP rats present a significant downregulation of miR-141 (71%), miR-200a (50%), miR-200b (60%) and miR-429 (59%). [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]
In isolated glomeruli, of 16-wk-old LP animals, miR-141, miR-200a, miR-200b and miR-429 were significantly down-regulated compared to NP offspring (Figure 9). [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]
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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[+] score: 14
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]
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]
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]
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]
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[+] score: 13
miR-429 was indicated to regulate 26 downregulated DEGs (P=1.52×10 [−10]), and miR-200a and miR-141 regulated 23 downregulated DEGs each, with P-values of 8.7×10 [−8] and 1.4×10 [−8], respectively. [score:9]
However, no targets of miR-200a, miR-429 and miR-141 were observed in the cholesterol metabolism -associated DEGs observed in the present study, which may be attributed to the small sample size of the microarray used. [score:3]
miR-429, miR-141 and miR-200a belong to the same miR-200 family. [score:1]
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[+] score: 11
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]
7 miRNAs that met the criteria ofLog2 fold change>1 and P value<0.05 were represented in blue dots and shown in Table 3. Among them, miR-664, miR-141, miR-145, miR-148b_MM2, miR-200a showed higher expression in the caput while miR-327 and let-7c in the cauda. [score:3]
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]
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]
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[+] score: 10
analysis of the hypertrophy markers ANF and BNP in transfected NRVMs showed that miR-139–5p and miR-374 mimics markedly increased the expression of ANF and BNP, while miR-324–5p, miR-153, and miR-141 mimics did not significantly affect the expression (unpublished data). [score:5]
Pten is directly targeted by miR-486 [24], miR-29a [60], and miR-141 [61]. [score:4]
We attempted to verify the effects of these six miRNAs (miR-185, miR-139–5p, miR-374, miR-324–5p, miR-153, and miR-141) on myocardial hypertrophy. [score:1]
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[+] score: 10
Cluster III included miR-141 and miR-376a and had increased expression at P0 and then a decreased expression at P2 compared to E20. [score:4]
ISH confirmed the localization to endocrine and exocrine tissue (Fig. 3 and Fig. S3); however, miR-141 was only weakly expressed in endocrine cells and predominantly found at P0 and P2 in exocrine cells. [score:3]
Interestingly, at E20 most of the miRNAs (except miR-141) were expressed in both exocrine and endocrine tissue. [score:3]
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[+] score: 7
It has also been demonstrated that [45], in inflammatory intestinal mucosa of CD patients and experimental colitis mice, the overexpression of CXCL12 β may promote immune cell infiltration and induce the morbidity of IBD in human and mice; intracolonic administration of pre-miR-141 may inhibit colonic CXCL12 β expression in mice and block immune cells trafficking into the inflamed sites, thereby significantly alleviating intestinal inflammation, which represents a promising approach that may be valuable for the treatment of CD. [score:7]
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[+] score: 6
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]
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]
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[+] score: 5
Notably, cardiac-specific miR-1, miR-133, miR-208 and miR-499 were all suppressed by two or more orders of magnitude [34], [35], as were the stemness and cell cycle repressors miR-141 and miR-137 [36]; in contrast, the proliferative miRNAs, miR-222 [37], increased dramatically in MDCs, and miR-221 was undetectable in myocytes but highly expressed in MDCs (Figure 5D). [score:5]
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[+] 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: 4
Studies found that miR-141, miR-200b and miR-205 can prevent TGF-β -induced EMT by downregulating ZEB1 and ZEB2, the two major transcriptional repressors of E-cadherin [15], [16]. [score:4]
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[+] score: 4
miR-141, miR-200a, miR-192, and miR-205 are upregulated in patients with hypertensive glomerulosclerosis [43]. [score:4]
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[+] 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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[+] score: 4
In the context of development, higher detected levels of miRNA in colostrum whey are interesting because miR-143, miR-148b-3p, and miR-141 are known to regulate intestinal function [41], [42] and miR-107 and miR-370 are known to modulate carbohydrate and lipid metabolism [27], [33]. [score:3]
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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That is, miR-140, miR-31, miR-875-5p and miR-141 were expressed mainly during tooth morphogenesis identified at embryonic day 16 (E16), whereas miR-689, miR-720, miR-711 and miR-455 were prevalent at the cytodifferentiation stage (E18) [8]. [score:3]
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[+] score: 3
Moreover, altered expressions of miR-18a, miR-124, miR-343-3p, miR-16, miR-141, miR-182, and miR-200a in the brain tissue of suicidal patients have been reported [6]. [score:3]
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[+] score: 3
Other miRNAs from this paper: rno-mir-22, rno-mir-675
As a miRNA sponge, lncRNA H19 can attenuate the endogenous function of miR-22 and miR-141, both of which negatively correlate with the β-catenin expression, resulting in the activation of Wnt/β-catenin signaling [11]. [score:3]
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[+] 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]
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[+] score: 2
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-194-1, rno-mir-194-2, rno-mir-200c, 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
113 −0.23 161 −20.19 TRUE rno-miR-218a-5p MIMAT0000888 1 7mer-m8 −0.105 −0.156 162 −17.51 TRUE rno-miR-141-3p MIMAT0000846 1 offset 6mer −0.021 −0.022 141 −13.96 TRUE Identity: the name of the mature miRNA in miRBase v20 Accession: the mature accession id used in miRBase v20 Site No. [score:1]
By the same method, we found that MRAK081523 and Plxna4 had the same MREs for miR-218, miR-141, miR-98 and let-7. Plxna4 reportedly promotes tumour progression and tumour angiogenesis by enhancing VEGF and basic fibroblast growth factor signalling [44]. [score:1]
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[+] score: 2
Other miRNAs from this paper: rno-let-7f-1, rno-let-7f-2, rno-mir-146a, rno-mir-221, rno-mir-146b
Al-Khalaf HH Aboussekhra A MicroRNA-141 and MicroRNA-146b-5p Inhibit the Prometastatic Mesenchymal Characteristics through the RNA -binding Protein AUF1 Targeting the Transcription Factor ZEB1 and the Protein Kinase AKTJ Biol Chem. [score:2]
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[+] score: 2
In 3 μg/kg treated dogs miR-216b-5p and miR-141-3p were increased at some time points, but miR-216b-5p was not increased beyond the level of the vehicle treated dog and did not display consistent time dependent increases. [score:1]
MiR-141-3p and miR-216a-5p were increased beyond vehicle treated dogs and did not display consistent time dependent increases. [score:1]
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[+] score: 1
Moreover, several studies have successfully identified circulating miRNA -based biomarkers; for example, Mitchell et al. [13] found that miR-141 was highly elevated in serum from patients with prostate cancer and hypothesized that this miRNA may be useful as a diagnostic marker. [score:1]
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[+] score: 1
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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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]
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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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