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29 publications mentioning rno-mir-129-1

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-129-1. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 301
It showed the expression of endogenous IGF-1 mRNA and protein decreased in primary DRG neurons transfected with miR-129 mimic, while the IGF-1 expression was upregulated with miR-129 inhibitor. [score:10]
The results suggested that miR-129 directly inhibited IGF-1 expression by binding to a defined target sequence. [score:8]
It indicated that four miRNAs, including miR-129, miR-18a, miR-206, and miR-340-5p, might regulate the important nerve regeneration -associated gene IGF-1. To verify which one/ones of them were exact regulators, the wild-type and mutant 3′-UTR of IGF-1 sub-cloned into the luciferase reporter vector including single target site mutant (mut 1 and mut 2) and double target site mutant (mut 1&2) were constructed and inserted into the reporter plasmid (Fig.   2a). [score:7]
Furthermore, IGF-1 knockdown prevented an increase in proliferation and migration of SCs by miR-129 inhibitors, which indicated that IGF-1 knockdown could recapitulate the suppressing effects of miR-129 on SCs phenotypic modulation. [score:7]
Overexpression of miR-129 inhibited the neurite outgrowth, suggesting that miR-129/IGF-1 axis could regulate neurite outgrowth directly based on its autocrine effect. [score:7]
To identify the effect of miR-129 on the expression of IGF-1 in SCs, miR-129 mimic or inhibitor were respectively transfected into SCs, and the mRNA and protein expressions of IGF-1 were respectively testified. [score:7]
The qRT-PCR (Fig.   4d) and western blot analysis (Fig.   4e) showed the mRNA expressions of IGF-1 were significantly suppressed by over -expression of miR-129, whereas were significantly enhanced by silencing of miR-129. [score:7]
Conversely, miR-129 inhibitor induced increase in SCs proliferation was significantly abrogated by IGF-1 knockdown after SCs were co -transfected with miR-129 inhibitor and IGF-1 siRNA (Fig.   5d). [score:6]
Interestingly, the comparison between Figs.   1 and 2 suggested that the temporal expression profile of miR-129 was negatively correlated with that of IGF-1, suggesting miR-129 negatively regulated the IGF-1 expression. [score:6]
PBS (PBS vehicle only), IGF-1 (IGF-1 protein, 100 μg/ml), anti-NC (inhibitor control), anti-miR-129 (miR-129 inhibitor). [score:5]
Immunostaining with anti-NF200 or anti-S100β showing that both IGF-1 and miR-129 inhibitor significantly promoted axon outgrowth and SCs migration at 10 days after nerve injury, respectively (Fig.   8a, b), which demonstrated the promoting effects of miR-129 inhibitor on peripheral nerve regeneration in vivo. [score:5]
d SCs transfected with miR-129 inhibitor increased the neurite outgrowth of DRG neurons, while the effect was abrogated by co-transfection with miR-129 inhibitor plus IGF-1 siRNA in SCs. [score:5]
SCs transfected with miR-129 inhibitor increased the neurite outgrowth of DRG neurons, while the effect was abrogated by co-transfection with miR-129 inhibitor plus IGF-1 siRNA in SCs (Fig.   7d). [score:5]
Upregulation of IGF-1 secretion in SCs at the injury site by miR-129 could promote axonal regeneration indirectly (Fig.   8c). [score:5]
The expression change of IGF-1 at mRNA (d) and protein levels (e) in SCs transfected with miR-129 mimic (miR-129) and miR-129 inhibitor (anti-miR-129). [score:5]
miR-129 negatively regulated IGF-1 by directly targeting its 3′-UTR. [score:5]
Moreover, miR-129 over -expression induced decrease in IGF-1 secretion from SCs, but miR-129 inhibitor failed to show the same effect (Fig.   4f). [score:5]
Moreover, miR-129 was shown to inhibit IGF-1 expression due to IGF-1 mRNA degradation. [score:5]
The expression change of IGF-1 at mRNA (c) and protein levels (d) in DRG neurons transfected with miR-129 mimic (miR-129) and miR-129 inhibitor (anti-miR-129). [score:5]
c The proliferation rate of SCs transfected with miR-129 was significantly decreased while the proliferation rate of SCs transfected with miR-129 inhibitor was significantly increased compared with that of control (d), but was then rescued by co-transfection with miR-129 inhibitor plus IGF-1 siRNA (anti-miR-129+ si IGF-1). [score:4]
NC (mimic control), anti-NC (inhibitor control) Collectively, the results further demonstrated that miR-129/IGF-1 axis played an important role in the regulation of SCs proliferation and migration. [score:4]
NC (mimic control), anti-NC (inhibitor control) Collectively, the results further demonstrated that miR-129/IGF-1 axis played an important role in the regulation of SCs proliferation and migration. [score:4]
This study focused on the possible regulatory role of miR-129 targeting IGF-1 during peripheral nerve regeneration. [score:4]
EdU incorporation results showed that over -expression of miR-129 reduced the proliferation rate of SCs to less than 50% of the control value while silencing of miR-129 increased the proliferation rate of SCs to nearly 1.5 folds compared to the control value, suggesting that miR-129 could suppress SC proliferation (Fig.   5c). [score:4]
After IGF-1R knocking down in DRG neurons (Fig.   7b), the significant decrease of neurite outgrowth by miR-129 over -expression in SCs was abolished (Fig.   7c). [score:4]
miR-129/IGF-1 axis not only regulated neurite outgrowth of DRG neurons directly, but also modified the regenerative microenvironment by regulating SCs proliferation and migration. [score:4]
In contrast, SCs transfected with miR-129 inhibitor induced a significant increase in cell migration rate compared to SCs transfected with non -targeting negative controls. [score:4]
Our work provides new insight into miR-129 regulation of peripheral nerve regeneration by robust phenotypic modulation of neural cells and opens a novel therapeutic window for PNI by mediating IGF-1 production, which may provide further experimental basis for translation of the molecular therapy into the clinic. [score:4]
It suggested that miR-129 could also suppress SCs migration by down -regulating IGF-1 (Fig.   6a, b). [score:4]
Besides, miR-129 inhibitor -induced increase in SCs migration was significantly abrogated by IGF-1 knockdown (Fig.   6c). [score:4]
A parallel experiment that SCs knocking down IGF-1R co-cultured with DRG neurons added with miR-129 mimic and control, miR-129 inhibitor and control (Fig.   7e), revealed that IGF-1 secreted by DRG neurons similarly is important on SC biology. [score:4]
Moreover, what are the up-regulators of miR-129 following PNI? [score:4]
Primary SCs were transfected with miR-129 mimic and control, miR-129 inhibitor and control, respectively, by the above-described protocols, and then co-cultured with rat DRG neurons, which have been transfected with IGF-1R siRNA and control previously. [score:3]
The expressions of miR-129 in the injured sciatic nerve changed over time following sciatic nerve transection, which suggested that miR-129 might be involved in peripheral nerve regeneration. [score:3]
Following nerve injury, a silicone tube was implanted into the sciatic nerve gap, and miR-129 inhibitor (antagomir) was injected into the silicone tube. [score:3]
NC (mimic control), anti-NC (inhibitor control)The result of migration assay showed that SCs transfected with miR-129 mimic or IGF-1 siRNA induced a significant decrease in cell migration rate compared to SCs transfected with non -targeting negative controls. [score:3]
miR-129 suppressed SCs proliferation and migration. [score:3]
NC (mimic control), anti-NC (inhibitor control) a The migration rate of SCs transfected with miR-129 was significantly decreased. [score:3]
miR-129 inhibited IGF-1 secretion of SCs. [score:3]
NC (mimic control), anti-NC (inhibitor control), Mutant miR-129 (mutated miR-129 mimic) As noted above, IGF-1 is secreted partially by SCs following nerve injury and is noted as a crucial factor in SCs biology. [score:3]
g The expression of IGF-1 was not significantly affected by mutant miR-129 mimic both on mRNA level and protein level (h). [score:3]
NC (mimic control), anti-NC (inhibitor control), Mutant miR-129 (mutated miR-129 mimic) a Co-localization of IGF-1 and S100 in SCs. [score:3]
miR-129 inhibited IGF-1 secretion from SCs. [score:3]
NC (mimic control), anti-NC (inhibitor control) The result of migration assay showed that SCs transfected with miR-129 mimic or IGF-1 siRNA induced a significant decrease in cell migration rate compared to SCs transfected with non -targeting negative controls. [score:3]
e Transfection of miR-129 mimic or inhibitor in DRG neurons, respectively. [score:3]
Ang II increases expression of rat miR-129 in cultured vascular smooth muscle cells [45]. [score:3]
Primary SCs were transfected with IGF-1 siRNA and negative control, miR-129 mimic and control, miR-129 inhibitor and control, respectively. [score:3]
c Increase in cell migration of SCs transfected with miR-129 inhibitor (anti-miR-129) was rescued by cotransfection with IGF-1 siRNA (si IGF-1). [score:3]
Expression of miR-129 in DRGs (c) and proximal nerve stumps (d) following sciatic nerve transection. [score:3]
The rats were randomly divided into four groups (n = 6 each) to receive injection of a mixture of Matrigel (BD Biosciences, Billerica, MA) with purified IGF-1 protein (100 μg/ml; R&D Systems) or PBS vehicle only, and miR-129 inhibitor (antagomir, Ribobio) or corresponding control (Ribobio) both at a volume ratio of 1:1, respectively. [score:3]
To verify the correlation between miR-129 and IGF-1 expressions, the expression profiles of miR-129 in DRGs and the proximal nerve segment at 0 h, 1, 4, 7, and 14 days following nerve injury were investigated (Fig.   2c,d). [score:3]
Our work firstly investigated the target regulation of miR-129 in affecting regenerative microenvironment to further regulate the proliferation and migration of primary SCs, and neurite outgrowth of DRG neurons. [score:3]
NC (mimic control), anti-NC (inhibitor control) Adult rat mo del with sciatic nerve transection were applied to determine in vivo effects of miR-129/IGF-1 on cell behaviors of neural cells during sciatic nerve regeneration. [score:3]
a Immunostaining with anti-NF200 or anti-S100β showing that both IGF-1 and miR-129 inhibitor promoted axon outgrowth or SCs migration at 10 days after nerve injury, respectively. [score:3]
Human IL17A protein may also increase expression of human miR-129 in cultured human dermal fibroblasts [45]. [score:3]
Primary SCs were transfected with miR-129 mimic and control, miR-129 inhibitor and control, respectively, and then co-cultured with DRG neurons, which have been transfected with IGF-1R siRNA and control previously (Fig.   7a). [score:3]
For parallel experiment on SC migration, DRG neurons were transfected with miR-129 mimic and control, miR-129 inhibitor and control, respectively. [score:3]
f IGF-1 secretion was reduced from SCs transfected with miR-129 mimic (miR-129) but was increased from SCs transfected with miR-129 inhibitor (anti-miR-129). [score:3]
DRG neurons transfected with miR-129 inhibitor increased the migration of SCs, while the effect was not significant in SCs transfected with IGF-1R siRNA. [score:3]
The relative expression of miR-129 was quantified with stem-loop RT primers (Ribobio) according to manufacturer’s instructions and normalized against the U6 level. [score:2]
Collectively, IGF-1 was shown to be negatively regulated by miR-129 at post-transcriptional level. [score:2]
miR-129/IGF-1 axis regulates proliferation of SCs. [score:2]
These data suggested that miR-129/IGF-1 axis regulated neurite outgrowth from DRG neurons. [score:2]
e Migration of SCs was decreased in co-cultures SCs with IGF-1R knocking down and DRG neurons with miR-129 mimic and control, but no change in co-culture with SCs transfected with IGF-1R siRNA. [score:2]
c Schematic diagram showing that miR-129/IGF-1/IGF-1R regulated regenerative microenvironment in the injured sites of sciatic nerve and DRG tissues following PNI Growing interests of PNI have fueled exploration of therapeutic approaches that promote spontaneous nerve regeneration. [score:2]
These indicate the effects of IGF-1 knockdown on SCs are similar to the effects of miR-129 mimics. [score:2]
c Schematic diagram showing that miR-129/IGF-1/IGF-1R regulated regenerative microenvironment in the injured sites of sciatic nerve and DRG tissues following PNI IGF-1 is important for the PNS response to injury and beneficial to axonal regeneration [12]. [score:2]
There was no change in DRG neurons transfected with IGF-1R siRNA, suggesting that the regulation of miR-129/IGF-1 axis was IGF-1R dependent. [score:2]
In the present work, our data provided evidence for a novel mechanism of regulating IGF-1/IGF-1R signaling in neurons and SCs by miR-129 and suggest a functional role of this miRNA, broadly, in injured neurons, and the pathogenesis of PNI. [score:2]
To investigate the regulatory mechanisms of IGF-1, our data from a dual-luciferase reporter assay confirmed that IGF-1 was an exact target gene of miR-129 through directly binding to IGF-1 3′-UTR. [score:2]
It indicates that the regulation of injury -induced secretion of IGF-1 by miR-129 plays crucial roles in the regenerative microenvironment following PNI. [score:2]
The results of mutated miR-129 mimic further confirmed the regulation of IGF-1 by miR-129 (Fig.   4g, h). [score:2]
The miR-129 expression in the proximal nerve segment was significantly decreased at 1, 4, 7, and 14 days following nerve injury as compared to that at 0 h (control). [score:2]
miR-129/IGF-1 axis regulates migration of SCs. [score:2]
miR-129 was an upstream regulator for IGF-1.. [score:2]
Our data showed that miR-129/IGF-1 axis also regulates the injury -induced acceleration in injured neurons. [score:2]
miR-129/IGF-1 axis regulates neurite outgrowth from DRG neurons. [score:2]
However, the accelerated growth of axon was blocked in miR-129 mimic transfected neurons. [score:1]
This interesting finding provided further evidence that IGF-1 was a functional mediator of miR-129. [score:1]
miR-129/IGF-1 axis is also important in the pre-lesion experiment and in vivo mo del, which would provide more clinical values regarding the application of IGF-1 or anti-miR-129 in patients with peripheral neural injury. [score:1]
In vivo effects of miR-129/IGF-1 axis on axon outgrowth and SCs migration. [score:1]
b The relative luciferase activity was analyzed after the wild-type or mutant IGF-1 3′-UTR reporter plasmid co -transfected into HEK 293T cells with miR-129 mimic (miR-129) or mimic control (NC). [score:1]
To investigate the effects of miR-129 on the expression of endogenous IGF-1 in DRG neurons, qRT-PCR (Fig.   3c) and western blot (Fig.   3d) were applied. [score:1]
Fig. 6 a The migration rate of SCs transfected with miR-129 was significantly decreased. [score:1]
Mutated miR-129 mimic was used to confirm the specific effect by miR-129. [score:1]
We firstly explored the role of miR-129/IGF-1 axis in DRG neurons. [score:1]
Fig. 8Effects of miR-129/IGF-1/IGF-1R pathway on neurite outgrowth in DRG neurons and SCs in vivo mo del. [score:1]
Fig. 2 a Sketches of the construction of wild-type or mutant IGF-1 3′-UTR reporter plasmid for miR-129. [score:1]
Similarly, the decrease of miR-129 was less dramatic in DRGs than that in the proximal nerve segment. [score:1]
We noted that miR-129 significantly reduced the luciferase activity of the 3′-UTR of IGF-1 (Fig.   2b). [score:1]
c Immunostaining with anti-β-Tubulin III showing that neurite outgrowth was decreased in co-cultured SCs transfected with miR-129 mimic and DRG neurons transfected with control siRNA, but no change in co-culture with DRG neurons transfected with IGF-1R siRNA. [score:1]
U6 served as internal reference a Sketches of the construction of wild-type or mutant IGF-1 3′-UTR reporter plasmid for miR-129. [score:1]
The regrowth effect was abolished in miR-129 mimic transfected DRG neurons. [score:1]
Effects of miR-129/IGF-1/IGF-1R pathway on neurite outgrowth in co-culture system of DRG neurons and SCs. [score:1]
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2
[+] score: 48
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]
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]
Dcn mRNA, a target gene of miR-129, encodes a protein that regulates cell cycle. [score:4]
In the 26-week group, the expression of miR-129 and miR-130b were decreased, while miR-141 was increased (Figure  10c). [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]
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]
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]
Among the six miRNAs that selected by STEM analysis, 4 miRNAs (most of the pathways were enriched by the targets of miR-129, miR-130a and miR-130b. [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]
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]
Notably, regulation of the pathways and GOBPs were strongly associated with miR-129, miR-130a and miR-130b. [score:2]
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3
[+] score: 37
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]
Compared with the control group, 16 miRNAs were upregulated, while 13 miRNAs were downregulated in the ASH group, where miR-129 and miR-199a-3p exhibited the greatest upregulation and downregulation, respectively, of the miRNAs. [score:12]
The unique miRNA expression patterns distinguishing the ASH group from the control group were composed of six downregulated (miR-199a-3p, miR-214, miR-93, miR-146a, miR-191 and let-7b) and six upregulated (miR-129, miR-490, miR-21, miR-503, miR-183 and miR-185) miRNAs. [score:9]
For instance, miR-129 has been reported to be associated with gastric cancer (25), thyroid cancer (26) and bladder cancer (27). [score:1]
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4
[+] score: 31
The PicTar algorithm identified 202 downregulated mRNAs which according to Ortis' study are potential targets for either of the above-mentioned upregulated miRNAs, and 36 upregulated mRNAs the possible targets for downregulated miR-129 (Table 4). [score:17]
Eight miRNAs from the PCR-confirmed 11 miRNAs, are common to both in vitro and in vivo inflammation conditions; 7 upregulated (miR-21, miR-98, miR-27a, miR-143, let-7d, miR-126 and miR-22) and one (miR-129) downregulated (Table 3). [score:7]
Using quantitative PCR -based high throughput analysis, we have confirmed upregulation of 7 (miR-21, miR-98, miR-27a, miR-143, let-7d, miR-126, and miR-22) and downregulation of 1 (miR-129) miRNAs out of the 26 activated miRNAs identified in our settings. [score:7]
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5
[+] score: 21
The expression of miR-320, miR-129* and miR-342-3p was significantly down-regulated by RDX. [score:6]
MiRNAs Target Genes Names Regulation Up Down miR-135a Up KIAA1033, CEP350, ROCK2 miR-320 Down BANP, CALD1, POLE4 miR-98 Up SULF1 miR-129* Down BANP, FAM82A2 miR-27ab Up HMGCR, LITAF, NPTX2 CALD1, C5orf13, KIAA1033 miR-342-3P Down VGF KIAA1033 miR-7a Up SLC38A2 POLE4, SLC35E4, C5orf13 miR-674-5p Up VGF Biological functional analysis revealed that more than half (8) of the overlapped genes are involved in neurological diseases and nervous system function (Table 4). [score:6]
MiRNAs Target Genes Names Regulation Up Down miR-135a Up KIAA1033, CEP350, ROCK2 miR-320 Down BANP, CALD1, POLE4 miR-98 Up SULF1 miR-129* Down BANP, FAM82A2 miR-27ab Up HMGCR, LITAF, NPTX2 CALD1, C5orf13, KIAA1033 miR-342-3P Down VGF KIAA1033 miR-7a Up SLC38A2 POLE4, SLC35E4, C5orf13 miR-674-5p Up VGFBiological functional analysis revealed that more than half (8) of the overlapped genes are involved in neurological diseases and nervous system function (Table 4). [score:6]
MiR-320, rno-miR-129* and their targets were both repressed by RDX. [score:3]
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6
[+] score: 18
This overall pattern replicates key components of our earlier study (Strickland et al., 2011), which showed that a contusion injury down-regulates miR1, miR129, and miR124, and up-regulates miR21 and miR146a. [score:7]
miR-129 regulates cell proliferation by downregulating Cdk6 expression. [score:7]
Our previous study showed that miR1, miR124, and miR129 were significantly down-regulated following a spinal cord contusion, while miR146a and miR21 were transiently induced (Strickland et al., 2011), and that these miRNAs were sensitive to opioid analgesics like morphine (Strickland et al., 2014). [score:4]
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7
[+] score: 18
Thermo-sensitive miRNAs Fold change in miRNA Fold change in target mRNA Predicted gene targets Cell Type rno-miR-22-3P + 3.4 −13.5 Acly Spermatid rno-miR-22-5P + 1.8 −13.5 Acly Spermatid rno-miR-129-5P −1.9 + 8.5 selV Spermatocyte rno-miR-3560 + 2.1 −1.6 MCT2 Spermatocyte rno-miR-3560 + 2.1 −12.3 Txnrd1 Spermatocyte rno-miR-466c-5P + 1.5 −1.8 Prkar2B Spermatid Crytorchidism is a state wherein the loss of germ cells takes place by apoptosis leading to infertility, and transient testicular heating has been shown to provide reversible contraception in men [25] and temporary sterility in rats [26]. [score:5]
Thermo-sensitive miRNAs Fold change in miRNA Fold change in target mRNA Predicted gene targets Cell Type rno-miR-22-3P + 3.4 −13.5 Acly Spermatid rno-miR-22-5P + 1.8 −13.5 Acly Spermatid rno-miR-129-5P −1.9 + 8.5 selV Spermatocyte rno-miR-3560 + 2.1 −1.6 MCT2 Spermatocyte rno-miR-3560 + 2.1 −12.3 Txnrd1 Spermatocyte rno-miR-466c-5P + 1.5 −1.8 Prkar2B Spermatid The H & E stained testes sections of control and cryptorchid rat suggest that at 24 h there was negligible visible change in any stage of spermatogenesis and most of the stages were present (Fig.   1b), as in control (Fig. 1a). [score:5]
The study has identified Acly, selV, SLC16A7(MCT-2), Txnrd1 and Prkar2B as potential heat sensitive targets in germ cells, which may be tightly regulated by heat sensitive miRNAs rno-miR-22-3P, rno-miR-22-5P, rno-miR-129-5P, rno-miR-3560, rno-miR-3560 and rno-miR-466c-5P. [score:4]
Among various pathways affected significantly by heat stress, the study has identified Acly, selV, SLC16A7(MCT-2), Txnrd1 and Prkar2B as potential heat sensitive targets in germ cells, which may be under tight regulation of heat sensitive miRNAs, rno-miR-22-3P, rno-miR-22-5P, rno-miR-129-5P, rno-miR-3560, rno-miR-3560 and rno-miR-466c-5P, as predicted by miRDB tool. [score:4]
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8
[+] score: 13
Among the miRNAs, miR-214, miR-199a-5p, miR-150, miR-199a-3p, miR-351, miR-145, miR-764, miR-497 and miR-92b were upregulated, whilst miR-7a, miR-325-5p, miR-485, miR-708, miR-344-3p, let-7f, miR-26b, miR-129, miR-29c and let-7a were downregulated. [score:7]
Another two miRNAs, miR-199a-3p and miR-129, which were found differentially expressed in the present study, were also reported to reveal altered expression levels under diabetic conditions in other studies (26, 27). [score:5]
These miRNAs include miR-214, miR-199a-5p, miR-150, miR-351, miR-145, miR-92b, miR-7a, miR-485, miR-708, let-7f, miR-26b, miR-129, miR-29c and let-7a. [score:1]
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9
[+] score: 12
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-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-26a-1, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-106a, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-99a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-126a, mmu-mir-127, mmu-mir-145a, mmu-mir-146a, mmu-mir-129-1, mmu-mir-206, hsa-mir-129-1, hsa-mir-148a, mmu-mir-122, mmu-mir-143, hsa-mir-139, hsa-mir-221, hsa-mir-222, hsa-mir-223, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-122, hsa-mir-125b-1, hsa-mir-143, hsa-mir-145, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-129-2, hsa-mir-146a, hsa-mir-206, mmu-mir-148a, 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-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-129-2, mmu-mir-103-1, mmu-mir-103-2, rno-let-7d, rno-mir-335, rno-mir-129-2, rno-mir-20a, mmu-mir-107, mmu-mir-17, mmu-mir-139, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-125b-1, hsa-mir-26a-2, hsa-mir-335, mmu-mir-335, 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-17-1, rno-mir-18a, rno-mir-21, rno-mir-22, rno-mir-26a, rno-mir-99a, rno-mir-101a, rno-mir-103-2, rno-mir-103-1, rno-mir-107, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-127, rno-mir-139, rno-mir-143, rno-mir-145, rno-mir-146a, rno-mir-206, rno-mir-221, rno-mir-222, rno-mir-223, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, hsa-mir-486-1, hsa-mir-499a, mmu-mir-486a, mmu-mir-20b, rno-mir-20b, rno-mir-499, mmu-mir-499, mmu-mir-708, hsa-mir-708, rno-mir-17-2, rno-mir-708, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-486b, rno-mir-126b, hsa-mir-451b, hsa-mir-499b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-130c, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, hsa-mir-486-2, mmu-mir-129b, mmu-mir-126b, rno-let-7g, rno-mir-148a, rno-mir-196b-2, rno-mir-486
After 6 and 12 wks of E [2] exposure, 15 miRNAs were down-regulated, e. g., miR-22, miR-99a, miR-106a, miR-127, miR-499, and 19 miRNAs were-up-regulated, e. g., miR-17-5p, miR-20a, miR-21, miR-129-3p, miR-106a, miR-22, and miR-127. [score:7]
By 18 wks of E [2] treatment, the mammary glands were characterized by lobular involution and hyperplasia, and only 1 miRNA was down-regulated (miR-139) and 5 miRNAs were up-regulated (miR-20b, miR-21, miR-103, mir-107, miR-129-3p, and miR-148a). [score:5]
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10
[+] score: 11
We also identified differential expression of a number of miRNAs which target histone modification enzymes; miR-145 suppresses histone deacetylase 2 (HDAC2) [51], miR-129 is predicted to target HDAC2 mRNA and miR-29 targets HDAC4 mRNA [52]. [score:11]
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11
[+] score: 8
The over -expression of miR-29a, 23b, 23a, 1 and let7a in SMSP (1–6):Hy5 and miR-129*, 103, 483, 107 and 326 in CMCP (1–6):Hy3 have been observed. [score:3]
Only two-fold or nearly two-fold over -expression has been observed in some cases, mostly in miR-29a for SMSP and miR-129* for CMCP. [score:3]
In order to see the effective mature microRNA molecules, denaturing polyacrylamide gel electrophoresis was conducted followed by Northern Blotting using [32]P-labeled miR-23a, miR-129*, miR-1 and let7a specific LNA Probes. [score:1]
MiR-129* is under-expressed in the experimental samples compared to the control (Fig. 4, panel I). [score:1]
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12
[+] score: 8
Of these miRNAs, rno-miR-129-1-3p, rno-miR-153-3p, rno-miR-29b-3p, rno-miR-29c-3p and rno-miR-451-5p were down-regulated, whereas rno-let-7a-1-3p, rno-miR-322-5p, rno-miR-3574 and rno-miR-628 were observed to be highly upregulated with p < 0.01 (Fig.   3). [score:7]
9 miRNAs (rno-miR-129-1-3p, rno-miR-153-3p, rno-miR-29b-3p, rno-miR-29c-3p, rno-miR-451-5p, rno-let-7a-1-3p, rno-miR-322-5p, rno-miR-3574 and rno-miR-628) showed statistically significant change. [score:1]
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13
[+] score: 8
We found that up-regulated miRNAs (miR-346, miR-135b, miR-30ab, miR-344, miR-18a, miR-99a, miR-210, miR-207, miR-18a, and miR-129) in ARDS were inversely correlated with the expression of their predicted targets such as Gabrb1, Mdh1, Eif2ak1, Fbln5, and Tspan8. [score:8]
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14
[+] score: 8
For example, miR-26b up-regulates the growth hormone levels by targeting lymphoid enhancer binding factor 1 (Lef-1) in GH3 cells, whereas miR-129-5p, miR-202 and two other miRNAs repress the human growth hormone receptor (GHR) expression levels in both normal and cancer cells [17, 18]. [score:8]
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15
[+] score: 7
As shown in Figure  2, levels of miR-129, miR-135a and miRNA-22 were significantly up-regulated in hippocampus in CCE rats, as compared to that in SCE rats (p < 0.05). [score:3]
To confirm findings from miRNA array study, five miRNAs (miR-129, miR-135a, miR-191, miRNA-22 and miR-26b) were chosen to examine their expression in rat hippocampus by quantitative RT-PCR (qRT-PCR). [score:3]
Notably, some miRNAs levels selectively affected in CCE rats, but not in CCA rats, such as miR-129, miR-135a and miR-22 in this study. [score:1]
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16
[+] score: 7
Other miRNAs from this paper: hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-139, hsa-mir-181c, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-140, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-296, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, hsa-mir-324, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-15b, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-19a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-181c, rno-mir-186, rno-mir-204, rno-mir-212, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, rno-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-181d, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-381, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-410, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Some miRNAs (miR-129-1-3p; miR-129-2-3p, miR-129-5p, miR181c-5p, miR181d-5p, miR-409a-5p, miR-655 and miR-874-3p) were up-regulated (Fig. 2, Supplementary Fig. S3A), whereas others (miR-296-5p, miR-500-3p and miR-652-3p) were down-regulated only in the chronic phase, while not being significantly altered during latency (Fig. 2, Supplementary Fig. S3B). [score:7]
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17
[+] score: 6
Interestingly, in 2014, Fu et al. reported that let-7a, miR-9, and miR-129-5p each had two target sites in FOXP2, and three mutant luciferase reporter constructs with mutations in one or two target sites were made. [score:6]
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18
[+] score: 3
Eleven miRNAs, including miR-145-5p, miR-34c-5p, miR-365-3p, miR-214-3p, miR-151, miR-27a, miR-153-5p, miR-365-3p, miR-33-5p, miR-217-5p and miR-129-5p, were differentially and significantly expressed (P < 0.05; Figure 2B). [score:3]
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[+] score: 3
Majority of the dysregulated microRNAs e. g. miR-380, miR-207, miR-79, miR-129, miR-153, miR-183, etc. [score:2]
Circulating levels of miR-129 and miR-142 were reduced in congestive heart failure [59, 60]. [score:1]
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20
[+] score: 3
Some of the differentially expressed miRNAs were previously reported (miR-223, miR-129, and miR-92) [4, 5], which support our results. [score:3]
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21
[+] score: 3
Six candidate miRNAs that are predicted to target caspase-3 (let-7, miR-138, miR-30b, miR-129, miR-203, and miR-219-5p) and have an aggregate Pct greater than 0.2 were selected (Fig.   1c). [score:3]
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[+] score: 2
miR-125b, miR-146, miR-150, miR-199a, miR-21, miR-129, miR-341 and miR-451 have been confirmed to play an important role in the different developmental stages of the cardiovascular system (4– 18). [score:2]
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23
[+] score: 1
Additionally, transfection of isolated adult rat cardiomyocytes with a set of fetal miRNAs (miR-21, miR-129, and miR-212) induced cellular hypertrophy and activation of a fetal gene program [117]. [score:1]
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24
[+] score: 1
Finally, there is mixed support for 7 of the miRNAs we reported (mir-129-1, miR-15b-3p, mir-204, miR-29c-3p, miR-301b-3p, miR-495, and mir-9a-2), with some studies showing changes consistent with our data, and other studies showing changes opposite those of our study (15, 31– 33, 38– 47). [score:1]
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[+] score: 1
Old age -associated miRNAs showed enrichment in pathways related to endocrine system disorders (miR-129-1, miR-375, miR-223, miR-664, miR-29b, miR-34a), cancer (miR-223, miR-29b, miR-375, miR-96), and cellular movement/invasion of cells (miR-29b, miR-29c, miR-7a, miR-96, miR-34a, miR-375). [score:1]
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[+] score: 1
Other miRNAs from this paper: rno-mir-129-2, rno-mir-142, rno-mir-146a, rno-mir-206
Among them, p values of miR-129-5p and miR-142-5p were both less than 0.01, being 0.0012 and 0.000058, respectively. [score:1]
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[+] score: 1
We began by measuring the levels of several miRNAs reportedly associated with cardiovascular diseases, including mir-129, mir-106, mir-26a, mir-20, mir-197, mir-17, mir-27 and mir-30d, 24, 25, 26, 27, 28, 29 in cardiomyocytes under both normal and high-glucose conditions. [score:1]
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[+] score: 1
We were unable to detect reproducible changes in the levels of miR-29b, miR-129-1* (currently annotated miR-129-1-3p), miR-484 and miR-488 (ESM Fig.   3). [score:1]
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29
[+] score: 1
let-7d*, miR-125b-2*, -1261, -1299, -130a, -1321, -208a, -22*, -23a, -27a*, -320b, -320d, -30c, -340, -422a, -423-3p, -488, -502-5p, -549a, -574-3p, -574-5p, -617, -627, -886-5p, -92a and -93* were unique for acute stroke while let-7a, let-7g, miR-129-5p, -192-5p, -196a*, -26b, -30b, -30e*, -370, -381, -493*, -525-5p, -652, -920, -933 and -96 were unique for “recovered” stroke patients (Figure 3; highlighted in bold). [score:1]
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