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22 publications mentioning rno-mir-100

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-100. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 223
For that purpose, we constructed lentiviral vector expressing the inhibitory oligonucleotides of miR-100 (miR100 -inhibitor) to specifically knock down the endogenous expression of miR-100. [score:10]
The results showed that the mRNA expression level of miR-100, presumably up-regulated upon apoptosis, was significantly down-regulated by knocking down IGF1R in RGC-5 cells (Figure  1D). [score:10]
The results of qRT-PCR showed that the endogenous expression level of miR-100 was significantly and specifically down-regulated by miR100 -inhibitor (Figure  3A, *: P <0.05). [score:8]
The RGC-5 cells with down-regulated miR-100 extended the peripherals to be long and neurite-like processes, whereas the cells without miR-100 downregulation kept original morphology of progenitor cell with short peripheral processes (Figure  4A). [score:7]
Our results demonstrated that down -regulating miR-100 did not alter the expression of Thy-1. However, miR-100 downregulation in RGC-5 cells significantly increased the phosphorylation in ERK1/2, AKT and TrkB, while keeping the total protein levels of ERK1/2, AKT and TrkB unchanged (Figure  5B-D, *: P <0.05). [score:7]
Luciferase assay confirmed that IGF1R was directly regulated by miR-100 in RGC-5 cells, and siRNA -mediated IGF1R knockdown activated AKT protein through phosphorylation, down-regulated miR-100, therefore exerted a protective effect on RGC-5 apoptosis. [score:6]
In the present study, not only did we show an active change in expression profile of miR-100 upon H [2]O [2] -induced apoptosis, but we also demonstrated that down-regulation of miR-100 had a protective effect on RGC-5 apoptosis. [score:6]
However, to elucidate the exact molecular interaction between miR-100 and TrkB/Akt/ERK pathways in protecting retinal ganglion apoptosis, future experiments of blocking TrkB or its downstream pathways upon the inhibition of miR-100 would provide solid evidence on direct targeting of miR-100 on anti-apoptotic pathways in retinal ganglion cells. [score:6]
The coding sequences were then amplified and cloned into pCDH-CMV-MCS-EF1-coGFP constructs (System Biosciences, USA) to construct miR-100 inhibitor vector (miR100-Inhibitor), miR-100 mimics vector (miR100 -mimics) and non-specific miRNA vector (miR-NC). [score:5]
Interestingly, our experiment also showed that knocking down IGF1R was able to down-regulate miR-100. [score:5]
Our results demonstrated that miR-100 was significantly up-regulated, and also in a dose -dependent manner by the application of H [2]O [2] in RGC-5 cells (Figure  2C, *: P <0.05). [score:4]
In the present study, we utilized an in vitro culture system to induce RGC-5 apoptosis through H [2]O [2] and found that miR-100 was up-regulated by H [2]O [2] in a dose -dependent manner. [score:4]
and qRT-PCR showed H [2]O [2] induced apoptosis and up-regulated miR-100 in a dose -dependent manner in RGC-5 cells. [score:4]
Figure 2 H [2] O [2] induced apoptosis and upregulated miR-100 in RGC-5 cells. [score:4]
Thus, it is likely that miR-100 downregulation may serve a role of TrkB agonist to exert a protective effect on H [2]O [2] -induced apoptosis in RGC-5 cells. [score:4]
Downregulation of miR-100 phosphorylated AKT/ERK/TrkB pathways in RGC-5 cells. [score:4]
Conversely, lentiviral -mediated miR-100 down-regulation protected H [2]O [2] induced apoptosis, promoted neurite growth and activated AKT/ERK and TrkB pathways through phosphorylation. [score:4]
This hypothesis was further supported by our results showing miR-100 down-regulation promoted neurite growth, possibly induced neural differentiation in RGC-5 cells, as TrkB activation is known to induce maturation in retina [29]. [score:4]
Downregulation of miR-100 reduces H [2]O [2] induced apoptosis and promoted neurite growth in RGC-5 cells. [score:4]
The effect of pre-treating RGC-5 cells with miR-100 down-regulation on oxidative stress induced apoptosis was then examined by. [score:4]
H [2]O [2] induced apoptosis and upregulated miR-100 in RGC-5 cells in a dose -dependent manner. [score:4]
Quantification results demonstrated that the percentage of apoptotic cells reduced from 55.5% in control RGC-5 cells to around 30% in cells with miR-100 down-regulation (Figure  3C, *: P <0.05). [score:4]
Figure 4 Downregulation of miR-100 promoted neurite growth in RGC-5 cells. [score:4]
We found that microRNA 100 (miR-100) was specifically upregulated in RGC-5 cells upon apoptosis. [score:4]
This result suggests that, instead of being downstream target of miR-100, IGF1R might be mutually interacted with miR-100 in regulating RGC apoptosis, acting through miR-100 itself or its upstream pathways. [score:4]
Our results of TUNEL staining showed that significantly less apoptosis were observed in miR-100 down-regulated RGC-5 cells than in control RGC-5 cells (Figure  3B). [score:4]
Figure 3 Downregulation of miR-100 protected apoptosis in RGC-5 cells. [score:4]
Interestingly, once the culture period was extended to 14 days after lentiviral transfection, we discovered that the morphology of RGC-5 cells was dramatically modified by miR-100 down-regulation. [score:4]
RGC-5 cells were pre -treated with lentiviral vector of miR100 -inhibitor, or its non-specific miRNA vector (miR-NC) for 24 hours, followed by H [2]O [2] (400 μM) treatment for another 24 hours. [score:3]
In that experiment, RGC-5 cells were transfected with either miR100 -inhibitor, or its non-specific miRNA (miR-NC) for 24 hours. [score:3]
In retina, miR-100 was found to be associated with diabetic retinopathy, a common retinal disease leading to total blindness [26]. [score:3]
org/), we noticed that, insulin-like growth factor 1 receptor (IGF1R) was a likely target of rat miR-100 (Figure  1A). [score:3]
In order to do that, RGC-5 cells were pre -treated with either miR100 -inhibitor or miR-NC for 24 hours, followed by H [2]O [2] (400 μM) treatment for another 24 hours. [score:3]
Finally, we examined the effect of knocking down IGF1R on miR-100 regulation and RGC-5 apoptosis. [score:3]
It has been commonly shown in the literature that miR-100 is an active factor in cancer regulation, modulating carcinoma development, metastasis or apoptosis [25, 27]. [score:3]
In retina, though miR-100 is expressed, little is known of its molecular mechanism [28]. [score:3]
The oligonucleotides of rno-miR-100 inhibitor, rno-miR-100 mimics and non-specific control were puchased from Ribo-Bio (Ribo-Bio, Shanghai, China). [score:3]
Down -regulating miR-100 is an effective method to protect H [2]O [2] induced apoptosis in RGC-5 cells, possible associated with IGF1R regulation. [score:3]
We then investigated the anti-apoptosis effect of down -regulating miR-100, as well as the association between miR-100 down-regulation and apoptosis-related pathways, Akt/ERK/TrkB and IGF1R, in retina ganglion cells. [score:3]
RGC-5 cells were pre -treated with miR100 -inhibitor, or miR-NC for 24 hours, followed by H [2]O [2] (400 μM) treatment for another 24 hours. [score:3]
We then looked at the effect of H [2]O [2] -induced apoptosis on the expression level of miR-100 in RGC-5 cells. [score:3]
The transfection of miR-100-Inhibitor or miR-NC into RGC-5 cells was conducted by a Lipofectamine 2000 reagent according to manufacturer’s recommendation (Invitrogen, USA). [score:3]
The method of down -regulating miR-100 might help to further our understanding on the mechanisms of degeneration and regeneration in retina tissues. [score:2]
However, the function role of miR-100 in mediating retinal development or pathology remains elusive. [score:2]
MicroRNA-100 (miR-100), a member of miR-99 family (including miR-99a, miR-99b, miR-100), is a key apoptotic regulator in various cell types [24, 25]. [score:2]
To evaluate the effect of down -regulating miR-100 on RGC-5 apoptosis, we pre -treated RGC-5 cells with either miR100 -inhibitor or miR-NC for 24 hours, followed by H [2]O [2] (400 μM) treatment for another 24 hours. [score:2]
Also in the present study we showed that, during H [2]O [2] -induced apoptosis, down -regulating miR-100 activated TrkB signaling pathways and its downstream Akt/ERK pathways, through phosphorylation. [score:2]
Downregulation of miR-100 reduces H [2]O [2] induced apoptosis and promoted neurite growth in RGC-5 cellsWe then investigated whether miR-100 played a functional role in modulating H [2]O [2] -induced apoptosis in RGC-5 cells. [score:2]
Overall, our study identified a novel regulator, miR-100 in modulating apoptosis in retinal ganglion cells. [score:2]
gov/ij/) confirmed the effect of down -regulating miR-100 on promoting neurite length in RGC-5 cells (Figure  4B, *: P <0.05). [score:2]
Figure 5 Effects of down -regulating miR-100 on AKT/ERK/TrkB pathways in RGC-5 cells. [score:2]
IGF1R was involved in miR-100 regulation in RGC-5. Discussion. [score:2]
The efficiency of down -regulating miR-100 by lentivirus was verified by qRT-PCR. [score:2]
H [2]O [2] induced apoptosis and upregulated miR-100 in RGC-5 cells in a dose -dependent mannerFirst, we investigated the effect of oxidative stress on RGC-5 cell apoptosis. [score:2]
Along with our early results demonstrating the functional association between miR-100 and Akt/ERK/TrkB pathways, a much more complex molecular network might be involved in the regulation of miR-100 in retina. [score:2]
We then investigated the intracellular signaling pathways that might be involved in the protection of miR-100 down-regulation on RGC-5 apoptosis. [score:2]
We then speculated IGF1R might be directly involved in the modulation of miR-100 on RGC-5 apoptosis. [score:2]
A mutant (MT) 3’-UTR of IGF1R (with modified binding site to rno-miR-100, Figure  1A) was also created by Site-Directed Mutagenesis Kit (SBS Genetech, China). [score:2]
All three vectors were co -transfected with β-galactosidase and miR-100 mimics (Ribo-Bio, Shanghai, China) into HEK293 cells in 6-well plates by using Lipofectamine 2000 according to the manufacturer’s protocol. [score:1]
Thus, these results highlighted a first ever report on functional role of miR-100 in retina. [score:1]
Retinal ganglion miR-100 Oxidative stress Apoptosis IGF-1 Retinal ganglion cells (RGCs) are a group of specialized sensory neurons in the central nervous system, rested in the inner layer of the retina. [score:1]
We thus applied a luciferase reporter assay to verify that miR-100 was directly binding IGF1R in RGC-5 cells (Figure  1B). [score:1]
The internal housing keeping genes were U6 for miR-100, and GAPDH for insulin-like growth factor 1 receptor (IGF1R) respectively. [score:1]
Through online bioinformatics search, as well as our luciferase assay and functional experiments (Figure  1), we further revealed that IGF1R was very likely to be directly involved in the modulation of miR-100 on H [2]O [2] -induced apoptosis in RGC-5 cells. [score:1]
Figure 1 miR-100 interacted with IGF1R in RGC-5 cells. [score:1]
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2
[+] score: 71
While miR-100 and miR-143 target NPR3 to downregulate its expression, both microRNAs were also observed to regulate MIR143HG promoter activity suggesting possible cross talk between the two NPR3 -targeting microRNAs. [score:11]
To further examine the interaction of miR-100 and miR-143 with predicted target sites on the promoter region of MIR143HG, mutations were introduced into selected transcriptional response elements that contain over 90% complementary base pair matching with the mature seed region of micro-143 and miR-100, namely −1504 bp and −2171 bp (miR-143 target sites), as well as −44 bp, and −1439 bp (miR-100 target sites) with respect to the transcription start site on the MIR143HG promoter region. [score:8]
Second, the upregulated miR-100 levels observed in multiple cardiovascular cells after knock down of miR-143 expression under both normoxic and hypoxic conditions (Supplemental data 1). [score:7]
Notably, miR-100 was found to target NPR3 3′UTR and is differentially upregulated in the plasma of heart failure patients, suggesting a plausible microRNA -based compensatory mechanism in response to cardiac overload. [score:6]
To examine the possible microRNA-directed transcriptional regulation of MIR143HG, miR-143 and miR-100 mimics were co -transfected with the pMIR143HG-containing vector and the relative strength of promoter activities in driving luciferase reporter expression in transfected cells was determined. [score:5]
This finding was corroborated by the observed upregulation of miR-100 in multiple cardiovascular cell lineages after knock down of the endogenous miR-143 levels using antagomiR-143 (Supplemental data 1). [score:5]
Nevertheless, the changes in MIR143HG promoter activities after treatment with miR-100 and miR-143 mimics reflect the complexity of microRNA-directed regulatory mechanisms in gene expression. [score:5]
This finding indicates that complementary base pairing of miR-100 and miR-143 with predicted motifs in the promotor region might play role(s) in microRNA-directed transcriptional modulation of the expression of MIR143HG. [score:4]
In recent published work, our group used multiple platforms to demonstrate the regulatory effects of miR-100 on the expression of NPR3 [13]. [score:4]
This hypothesis is supported by two lines of evidence, first, the observation of diminished regulatory effect of miR-100 and miR-143 on luciferase activity in cells that harbor mutations on the MIR143HG promoter. [score:3]
Feedforward regulation of miR-143 and miR-100 on the MIR143HG promoter activity. [score:2]
Figure 6 Schematic diagram of hypoxia -induced transcriptional activation of MIR143HG and the proposed microRNA directed transcriptional modification by miR-143 and miR100 in cardiac cells. [score:2]
Intriguingly, the promoter activity of MIR143HG was enhanced in the presence of exogenous miR-143, but was suppressed by the exogenous miR100 compared to scrambled controls (Fig.   4a). [score:2]
In the 2-Kb MIR143HG promoter region, 7 and 4 putative binding sites were identified for miR-143 and miR-100, respectively (Tables  2 and 3). [score:1]
Location Sequence alignment Transcriptional factors −44pMIR143HGmiR-1005′-C CCGCCTCG CCCCAA TACGGGGC-3′3′- GUGUUCAA GCCUAG AUGCCCAA-5′ GR-β, Pax-5, P53 and NFI/CTF −639pMIR143HGmiR-1005′-GCTGG GTCA GGATCTT CCCTG T-3′3′-GUGUU CAAG CCUAGAU GCCCA A-5′ TFII-I, STAT4, NF-κB, RelA and RAR-α −1439pMIR143HGmiR-1005′- CACAAGGC CCCG TG TG CT GC TG-3′3′- GUGUUCAA GCCU AG AU GC CC AA-5′ GR-α, AP-2αA, Pax-5 and P53 −2112pMIR143HGmiR-1005′- CACAAGCCTTCCCTA ACCCACC-3′3′- GUGUUCAAGCCUAGA UGCCCAA-5′ C/EBPβ The promoter position of the nucleotide with respect to the transcription start site (defined as position 0) that is aligned to the 3′ end of each putative miR-100 binding site in MIR143HG promoter region is indicated under the “Location” column. [score:1]
In the current study, the effects of miR-143 and miR-100 on MIR143HG and MIR100HG promoter activities suggest possible cross talk between the two microRNAs. [score:1]
The negative modulation of the transcriptional activity of miR-100 host gene, MIR100HG, was also observed when treated with exogenous miR-143 (Fig.   4b). [score:1]
Luciferase reporter analyses showed that miR-100 and miR-143 fail to modulate the luciferase activities in cardiac cells that harbor the corresponding mutated MIR143HG promoter constructs (Fig.   4a). [score:1]
Sequence analysis of the promoter region of MIR143HG revealed the presence of several specific sequence motifs (~6–7 nucleotides) that are complementary to mature miR-143 and miR-100. [score:1]
Figure 4Differential promoter activities of MIR143HG and MIR100HG in the presence of exogenous miR-100 or miR-143 in HCMa cells. [score:1]
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3
[+] score: 50
Furthermore, tissue miR-100 was downregulated after PH and SL but upregulated after AN, while plasma miR-100 was lower expressed after SL and AN but not after PH. [score:9]
These findings illustrate that plasma and tissue miRNA expression levels do not necessarily have to correlate (e. g. miRNA-466c) and that independent and differential, even counteracting, effects of surgery and anesthesia might add up to a very complex picture (e. g. tissue miRNA-100 is downregulated by SL, which encompasses surgery and anesthesia, but upregulated by AN alone). [score:9]
In plasma, miRNA upregulation was observed for miR-133a and miR-133b following PH and SL, whereas miR-100 and miR-466c were similarly downregulated following anesthesia and surgery. [score:7]
Downregulation of rno-miR-100 was statistically significant in the SL- and AN-group, while rno-miR-466c downregulation was significant in the PH- and SL-group. [score:7]
Comparing significantly deregulated miRNAs in the SL- and PH-group, we identified 10 miRNAs (rno-miR-100, rno-miR-105, rno-miR-1224, rno-miR-133a/b, rno-miR-383, rno-miR-466c, rno-miR-483, rno-miR-598-5p, and rno-miR-628) that showed similar expression changes in both groups at the same postoperative time point, while one miRNA (rno-miR-29a) was regulated in the opposite direction at the same time point. [score:6]
The expression levels of rno-miR-100 and rno-miR-466c were similarly downregulated following PH, SL, and anesthesia only compared to non -treated animals (Figure 2). [score:5]
Out of these miRNAs, two (rno-miR-100 and rno-miR-466c) were significantly upregulated following isoflurane anesthesia compared to untreated animals (1.97 fold and 1.88 fold expression change, respectively; p < 0.01 and p = 0.001). [score:5]
Therefore, we performed anesthesia controls in our study, and we identified miR-100 and miR-466c to be deregulated in liver tissue and plasma samples of these animals. [score:2]
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4
[+] score: 29
It was found that 8 miRNAs were significantly and consistently down-regulated in the hypertonic dialysate group (miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b), and within which miR-192, miR-194 and miR-200b were also down-regulated in the normal saline group (Table  3). [score:7]
The miRNA screen identified 8 significantly down-regulated miRNAs (miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b) and one highly up-regulated miRNA (miR-122) in the hypertonic dialysate group. [score:7]
The results demonstrated that in the hypertonic dialysate group, miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b were all significantly down-regulated whereas miR-122 was highly up-regulated (all P <0.05) (Figure  3). [score:7]
Compared with the control and saline groups, both miRNA microarray and real-time PCR analyses demonstrated that miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b were significantly down-regulated, and miR-122 was highly up-regulated in the hypertonic dialysate group. [score:6]
Several studies have demonstrated that miR-100, miR-152 and miR-497 are associated with the development of tumor and tumor metastasis [54- 56]. [score:2]
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5
[+] score: 28
To be specifically mentioned (fold change >2.5), miR-208, miR-19b, miR-133b and miR-30e were significantly upregulated and miR-99b, miR-100, miR-191a, miR-22 andmiR-181a-1 were significantly downregulated. [score:7]
The summary of the miRNAs significantly differentially expressed are provided in Table 1. Our study revealed the significant downregulation of miR-99 family (Fig. 2A,B) that comprises of three miRNAs such as miR-99a, miR-99b and miR-100, which are present in 11, 1, 8 chromosomes respectively. [score:6]
miR-100 IGF1R, Akt, mTOR The expression of miR-100 was highly downregulated during physiological hypertrophy. [score:6]
miR-99b, miR-100, miR-191a, miR-22 and miR-181a were significantly downregulated during hypertrophy (Fig. 2B). [score:4]
miR-100 was reported to be upregulated during heart failure by β-adrenergic receptor mediated repression of adult cardiac genes [22]. [score:4]
We found that miR-99, miR-100, miR-208, miR-181, miR-19 and many others were associated to cardiac hypertrophy and apoptosis. [score:1]
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6
[+] score: 21
More importantly, the miRNAs analyzed in this study not only included the miRNAs like Let-7a, miR-15b, miR24, miR-100 and miR-125 which may suppress the expression of cyclins A and B, and miRNAs such as Let-7a, miR24 and miR-125 which may regulate activity of CDK1, but also miRNAs such as miR-181a, miR-221 and miR-222 which can target CDK inhibitors [30– 32]. [score:10]
To investigate whether miRNAs have a role in the cell cycle regulation of splenocytes following aniline exposure, the expression of miRNAs, including Let-7a, miR-15b, miR24, miR-100, miR-125, miR-181a, miR-221 and miR-222 which are known to mainly control G2/M phase regulators [30– 32], was analyzed by using real-time PCR and the results are presented in Fig 7. Aniline exposure led to significantly decreased expression of Let-7a (decreased 82%), miR-15b (decreased 62%), miR24 (decreased 78%), miR-100 (decreased 63%), miR-125 (decreased 86%), whereas miR-181a, miR-221 and miR-222 increased by 155%, 78% and 56%, respectively, in comparison to controls (Fig 7). [score:5]
Real-time PCR analysis of miRNAs Let-7a, miR-15b, miR24, miR-100 and miR-125 (A), and miRNAs miR-181a, miR-221 and miR-222 (B) expression in rat spleens following aniline exposure. [score:3]
Therefore, greater decreases in Let-7a, miR-15b, miR24, miR-100 and miR-125 expression and significant increases in miR-181a, miR-221 and miR-222 levels in the spleens following aniline treatment may be mechanistically important in generalizing that aniline exposure leads to increased cyclin A, cyclin B, CDK1, and decreased p21, p27, thus triggering the splenocytes to go through G2/M transition. [score:3]
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7
[+] score: 21
Tsp-let-7 showed very low expression in NBL stage, whereas tsp-miRNA-100 was detected in rather high abundance at the same development stage. [score:4]
Since this miRNA was found by both sequencing and qPCR in the Ad stage, we have no doubt that tsp-mir-100 was indeed expressed at this stage. [score:3]
Further, MiR-100 and let-7, the two conserved miRNA in metazoa, play a role in regulation of developmental timing [18], [42], [45]. [score:3]
However, the probe for tsp-mir-100 did not show any signal with total RNA purified from the Ad stage; this was likely due to probe modification or other unidentified factors that prevented annealing of the probes with the targets (Fig. 6B). [score:3]
The following forward primers were designed to confirm the sequencing results of miRNAs that showed differential expression patterns: tsp-miR-100 5′-AAC CCG TAG ATC CGA ACT TGT GT-3′; tsp-let-7 5′-TGA GGT AGT AGG TTG TAT AGT T-3′; tsp-miR-228 5′-AAT GGC ACT GGA TGA ATT CAC GG-3′; tsp-miR-1 5′-TGG AAT GTA AAG AAG TAT GTA G-3′; tsp-miR-31 5′-AGG CAA GAT GTT GGC ATA GCT GA-3′; tsp-novel-108 5′-CTT GGC ACT GTA AGA ATT CAC AGA-3′; tsp-novel-83 5′-TTG AGC AAT TTT GAT CGT AGC-3′; tsp-novel-46 5′-TGG ACG GCG AAT TAG TGG AAG-3′; tsp-novel-86 5′-TGA GAT CAC CGT GAA AGC CTT T-3′; tsp-novel-21 5′-TCA CCG GGT AAT AAT TCA CAG C-3′. [score:2]
The TPM of tsp-miR-100-5p and tsp-miR-100-3p, tsp-miR-125-5p and tsp-miR-125-3p, tsp-miR-9-1-5p and tsp-miR-9-1-3p, tsp-miR-9-2-3p and tsp-miR-9-2-5p behaved in similar fashion (Fig. 4, Fig. 5A and Table S5). [score:1]
Five conserved miRNAs (tsp-miR-228, tsp-miR-100, tsp-let-7, tsp-miR-1 and tsp-miR-31) and five novel miRNAs (tsp-novel-108, tsp-novel-83, tsp-novel-46, tsp-novel-86 and tsp-novel-21) with relatively higher TPM values identified by sequencing were validated by qRT-PCR and Northern blot. [score:1]
The oligonucleotide probes used for hybridization are as follows: tsp-mir-100 probes: 5′ACACAA*GTTC*GGATCT*AC*GGGTT3′ tsp-let-7 probes: 5′AACTAT*ACA*ACCT*ACT*ACCTCA3′ tsp-novel-108 probes: 5′TCT*GT*GAATTCTT*ACA*GTGCCAAG3′ tsp-novel-83 probes: 5′GCTAC*GATC*AA*AATT*GCTCAA3′ (LNA (Locked nucleic acid) substitutions are indicated by a “*”). [score:1]
The oligonucleotide probes used for hybridization are as follows: tsp-mir-100 probes: 5′ACACAA*GTTC*GGATCT*AC*GGGTT3′ tsp-let-7 probes: 5′AACTAT*ACA*ACCT*ACT*ACCTCA3′ tsp-novel-108 probes: 5′TCT*GT*GAATTCTT*ACA*GTGCCAAG3′ tsp-novel-83 probes: 5′GCTAC*GATC*AA*AATT*GCTCAA3′ (LNA (Locked nucleic acid) substitutions are indicated by a “*”). [score:1]
The abundance of tsp-miRNA-100 was almost identical with that of tsp-let-7 in both Ad and ML stage, indicating that miRNA-100 may be more functional in NBL stage. [score:1]
Their homologs, tsp-miRNA-100 and t sp-let-7, were found throughout the life cycle of T. spiralis. [score:1]
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8
[+] score: 14
Of the 46 increased miRNA, sICAM-1 was the predicted target of 6 (miR-23b, miR-27a, miR-99a, miR-100, miR-324-5p, miR-363); PAI-1 was the predicted target of 4 (miR-30a, miR-30d, miR-182, miR-384-5p), E selectin the predicted target of 2 (miR-16; miR-195) and the alpha chain of fibrinogen the predicted target of miR-29c [26]. [score:9]
As depicted in Fig 6, among the miRNAs elevated in serum in our study, LPS has been shown to increase expression of miR-10a, miR-100, miR-508/511, miR-30c, and miR-125b in human fibroblast-like synoviocytes [41], increase expression of miR-146a in a human monocyte cell line [42], and increase miR-21 in cultured murine monocytes [43]. [score:5]
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9
[+] score: 13
In human muscle, diminished miR-99 and miR-100 expression predict the anabolic response to a resistance exercise bout, with reduced expression of these miR upregulating mTORC1 signaling (Zacharewicz et al., 2014). [score:8]
miR that regulate targets in the mTORC1 pathway (hsa-miR-16-5p, hsa-miR-26b-5p, hsa-miR-99a-5p, hsa-miR-100-5p, hsa-miR-128a-3p, hsa-miR-133a-3p, hsa-miR-199a-3p, hsa-miR-221-3p) were analyzed using TaqMan® microRNA Assays (Applied Biosystems, Foster City, CA, USA). [score:3]
Findings from the present investigation indicate that alterations of mTORC1 signaling following sustained CR are not regulated by the expression of miR-99a or miR-100-5p. [score:2]
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10
[+] score: 12
miR-100 targets AGO2, miR-199a-3p and miR-145 target ZEB2, miR-143 targets BCL2, and miR-199a-5p targets CDKN1B, which are 4 of 7 genes targeted by the rat miRNA signature in the present study. [score:11]
al, showed changes in miR-100, 199a-3p, 199a-5p, miR-143 and miR-145. [score:1]
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11
[+] score: 7
However, it should be noted that although miRNAs-including miR-352 in this paper and other miRNAs found in previous studies, such as miR-100, miR-155, miR-329, and miR-495- are important factors controlling FSS -induced collateral vessel growth 15– 17, the mechanism by which miRNAs expression is regulated remains unclear. [score:4]
More recently, several studies have demonstrated that a different miRNA expression profile is induced in collateral vessels of mice following femoral artery occlusion, and several miRNAs such as miR-100, miR-155, miR-329 and miR-495 were found to be important factors that control collateral vessel growth 15– 17. [score:3]
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12
[+] score: 5
The following conventions for miRNA naming are used: (i) The predicted stem-loop portion of the primary transcript is named by a 3 or 4 letter species prefix and a numerical suffix (e. g. hsa-mir-100 in Homo sapiens). [score:1]
Whereas, the name of the excised ~22 nucleotide sequence (mature miRNA) contains the same mir, prefix and suffix as stem-loop but with capital miR (e. g. hsa-miR-100). [score:1]
In some cases, the asterisk has been used to denote the less predominant form (e. g. hsa-miR-100*). [score:1]
and a prefixed species identifier (e. g. hsa-miR-100) [7, 37, 38]. [score:1]
The following conventions for miRNA naming are used: (i) The predicted stem-loop portion of the primary transcript is named by a 3 or 4 letter species prefix and a numerical suffix (e. g. hsa-mir-100 in Homo sapiens). [score:1]
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13
[+] score: 5
For example, miR-17 [12] and miR-100 [13] were up regulated while miR-10a [14] and miR-205 [15] were downregulated during the osteogenic differentiation in bone mesenchymal stem cells of rats (rBMSCs). [score:5]
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14
[+] score: 4
Out of the 14 miRNAs that were detected to be differentially expressed using NGS (Table  4), five (rno-let-7d-5p, rno-miR-100-5p, rno-miR-203a-3p, rno-miR-21-5p, rno-miR-320-3p) were represented on the TLDA-A, while nine (rno-miR-378a-3p, mmu-miR-5100, rno-miR-30e-3p, rno-miR-125b-2-3p, rno-miR-320-5p, rno-miR-3473, rno-miR-21-3p, rno-miR-455-5p, and hsa-miR-7641) were not. [score:3]
Similarly, miR-100-5p and let-7a-5p implicated in renal inflammation and nephritis may be tubular injury biomarkers specifically detected by NGS. [score:1]
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[+] score: 3
Other miRNAs from this paper: hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-100, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, hsa-mir-16-2, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-9-2, mmu-mir-145a, mmu-mir-181a-2, mmu-mir-184, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-205, mmu-mir-206, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-199a-2, hsa-mir-205, hsa-mir-181a-1, hsa-mir-214, hsa-mir-219a-1, hsa-mir-223, mmu-mir-302a, hsa-mir-1-2, hsa-mir-23b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-184, hsa-mir-206, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-103-1, mmu-mir-103-2, rno-mir-338, mmu-mir-338, rno-mir-20a, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-107, mmu-mir-17, mmu-mir-100, mmu-mir-181a-1, mmu-mir-214, mmu-mir-219a-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-372, hsa-mir-338, mmu-mir-181b-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-103-2, rno-mir-103-1, rno-mir-107, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-145, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-184, rno-mir-199a, rno-mir-205, rno-mir-206, rno-mir-181a-1, rno-mir-214, rno-mir-219a-1, rno-mir-219a-2, rno-mir-223, hsa-mir-512-1, hsa-mir-512-2, rno-mir-1, mmu-mir-367, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, rno-mir-17-2, hsa-mir-1183, mmu-mir-1b, hsa-mir-302e, hsa-mir-302f, hsa-mir-103b-1, hsa-mir-103b-2, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-219b, hsa-mir-23c, hsa-mir-219b, mmu-mir-145b, mmu-mir-21b, mmu-mir-21c, mmu-mir-219b, mmu-mir-219c, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Brain research 55 Henson B Bhattacharjee S O'Dee D Feingold E Gollin S 2009 Decreased expression of miR-125b and miR-100 in oral cancer cells contributes to malignancy. [score:3]
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[+] score: 3
The reference genes utilised were miRNAs with stable expression across samples according to BestKeeper: miR-22, miR-30a, miR-30c, miR-30e and miR-100. [score:3]
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[+] score: 3
Nine of the miRs (miR-200b-3p, miR-27a-3p, let-7a-5p, miR-21-5p, miR-10b-5p, miR-23b-3p, miR-221-3p, miR-100-5p, and miR-28-5p) were differently expressed at both 24 and 72 hours after reperfusion. [score:3]
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[+] score: 3
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
A comparison of effects of ACTH and DEX shows that both hormones increased the expression miRNA-181b, miRNA-672, and miRNA-100, and significantly decreased the levels of miRNA-92a, and miRNA-466b. [score:3]
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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-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-200c, 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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[+] score: 2
At 24 hours, five miRNAs (rno-miR-214, rno-miR-99a, rno-miR-363*, rno-miR-100 and rno-miR-340–5p) and at 48 hrs 6 miRNAs (rno-miR-34b, rno-miR-500, rno-miR-24-1*, rno-miR-29b, rno-miR-199a-3p, rno-let-7a) showed the most prominent dysregulation (P < 0.001) (Fig.   7B). [score:2]
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We found four microRNAs (LET-7, MIR-100, MIR-125, and MIR-126) that could detect teratomas and had previously been associated with oncogenic transformations (Gu et al., 2015, Wu et al., 2015). [score:1]
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Seeliger et al. profiled miRNAs in bone tissue from patients with osteoporotic fractures and identified five miRNAs, miR-21, miR-23a, miR-24, miR-100, and miR-125b that are highly associated with osteoporotic fractures [13]. [score:1]
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