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29 publications mentioning rno-mir-107

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-107. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 351
Down-regulation of CD31 and eNOS after up-regulation of miR-107 was offset by up-regulation of HIF-1β (Fig. 5 a, b, c), which showed the up-regulation of miR-107 would inhibit EPCs differentiation via inhibiting HIF-1β. [score:17]
The results from the present study have revealed that 1) miR-107 expression were increased in EPCs under hypoxic conditions; 2) up-regulation of miR-107 partly suppressed the EPCs differentiation induced in hypoxia, while down-regulation of miR-107 promoted EPCs differentiation; and 3) HIF-1β was the target for this pathway. [score:13]
Overexpression of miR-107 in EPCs prevents their differentiation via down-regulation of HIF-1β, while under expression of miR-107 in EPCs induces their differentiation via up-regulation of HIF-1β. [score:11]
Overexpression of miR-107 inhibited mRNA and protein expression of HIF-1β (a and b), miR-107 inhibitor increased HIF-1β expression (c and d) (*p<0.05 between groups). [score:11]
We found that down-regulation of miR-107 up-regulated CD31 and eNOS, which was offset by down-regulation of HIF-1β in hypoxic and normoxic conditions (Fig 5 d, e, f). [score:10]
[N: EPCs cultured under normoxic conditions; L: EPCs cultured under hypoxic conditions; N+H: EPCs infected with Lentiviral vector expressing miR-107 and cultured under normoxic conditions; L+H: EPCs infected with Lentiviral vector expressing miR-107 and cultured under hypoxic conditions; N+L: EPCs transfected with miR-107 inhibitor and cultured under normoxic conditions; L+L: EPCs transfected with miR-107 inhibitor and cultured under hypoxic conditions. [score:9]
Therefore, miR-107 may partly inhibit hypoxia induced HIF-1α overexpression and subsequently inhibit overexpression of HIF-1α induced EPC differentiation in hypoxic conditions. [score:9]
We demonstrated that the overexpression of miR-107 in EPCs would down-regulate the expression of mRNA or the HIF-1β protein. [score:8]
This is because lenti- HIF-1β increased endogenous HIF-1β expression, while lenti-miR107 reduced miR-107 direct target HIF-1β expression in EPCs. [score:8]
0040323.g004 Figure 4 The HIF-1β expression of the EPCs were tested by Q-PCR (a and c) and western blotting (b and d) after the up-regulation of miR-107 (a and b) and inhibition of miR-107 (c and d). [score:8]
The HIF-1β expression of the EPCs were tested by Q-PCR (a and c) and western blotting (b and d) after the up-regulation of miR-107 (a and b) and inhibition of miR-107 (c and d). [score:8]
To down-regulate the expression of miR-107, miR-107 inhibitor (Ambion, AM17000) was transfected into EPCs using Lipofectamine 2000 (Invitrogen, Carlsbad, CA). [score:8]
Conversely, knockdown of miR-107 in EPCs would up-regulate HIF-1β expression. [score:7]
In conclusion, the present study indicated that miR-107 is up-regulated in hypoxia to prevent EPC differentiation via its target HIF-1β. [score:6]
CD31 (a) and eNOS (b and c) expression of EPCs were determined after up-regulation of miR107. [score:6]
We found that up-regulation of miR-107 in EPCs substantially decreased HIF-1β expression (Fig 4 a and b), and vice versa (Fig 4 c and d). [score:6]
The EPCs were infected by Lentiviral vector expressing miR-107 to up-regulate miR-107. [score:6]
From these collective results we can conclude that miR-107 was up-regulated in hypoxic conditions to prevent EPC differentiation via its target HIF-1β. [score:6]
0040323.g003 Figure 3(1) Upregulation of miR-107 suppressed the differentiation of EPCs. [score:6]
Since our study suggests miR-107 is a negative feedback to hypoxia and HIF-1β is a target of miR-107, we believe that HIF-1β may be present in excess in normoxia in order to functionally decrease during the period at which miR-107 is up-regulated during hypoxic conditions. [score:6]
[N: EPCs cultured under normoxic conditions; L: EPCs cultured under hypoxic conditions; N+L: EPCs transfected with miR-107 inhibitor and cultured under normoxic conditions; L+L: EPCs transfected with miR-107 inhibitor and cultured under hypoxic conditions. [score:5]
CD31 (d) and eNOS (e and f) expression of EPCs were determined after inhibition of miR107. [score:5]
N+HH: EPCs infected with lentivirus carrying siRNA against both miR-107 inhibitor and HIF-1β cultured under normoxic conditions; L+HH: EPCs infected with lentivirus carrying siRNA against both miR-107 inhibitor and HIF-1β cultured under hypoxic conditions. [score:5]
From this it can be concluded that down-regulation of miR-107 would promote EPCs differentiation via up -regulating HIF-1β. [score:5]
Our findings indicate that miR-107 expression increases in EPCs and partly inhibits their differentiation in hypoxic conditions. [score:5]
These data suggest the overexpression of miR-107 in EPCs suppressed the differentiation of EPCs. [score:5]
[N: EPCs cultured under normoxic conditions; L: EPCs cultured under hypoxic conditions; N+H: EPCs infected with Lentiviral vector expressing miR107 and cultured under normoxic conditions; L+H: EPCs infected with Lentiviral vector expressing miR107 and cultured under hypoxic conditions. ] [score:5]
MiR107 suppress EPCs differentiation via down-regulation of HIF-1β. [score:5]
Some research using target prediction software has suggested that miR-107 targets 3′UTR of yak HIF-1α. [score:5]
When we overexpressed both miR-107 and HIF-1β in EPCs, the miR-107 -inhibited EPC differentiation was counteracted. [score:5]
Our present study agrees with these findings that HIF-1β is down-regulated post-transcriptionally by miR-107. [score:4]
After 14 days, the analysis of the differentiation revealed that the down-regulation of miR-107 promoted the differentiation of EPCs (Fig 3 d, e and f). [score:4]
Therefore it is possible that PI3K/Akt pathway inhibition may be the mechanism that regulates miR-107 modulated EPC differentiation, however, further research both in vitro and in vivo must be performed to validate this hypothesis. [score:4]
The target sequence was amplified with primers of miR-107 (Table 1A) and HIF-1β (Table 1B) and cloned into sites (BamHI/EcoRI) of expression vector pCDH-CMV-MCS-EF1-Puro (System Biosciences, Mountain View, CA, USA). [score:4]
Down-regulation of miR-107 inducing EPC differentiation was offset. [score:4]
The expression plasmids for hsa-miR-107 and HIF-1β were created [11]. [score:3]
However, it was unknown whether miR-107, the miR induced in response to low oxygen, would be overexpressed in hypoxic EPCs and subsequently affect the differentiation capacity of EPCs. [score:3]
Second, the effect of miR-107 overexpression on EPC differentiation is still unknown. [score:3]
The effects of miR-107 on HIF-1β expression in normoxia and hypoxia. [score:3]
Finally, there is no evidence as to which subunit of HIF, α or β, should be the target of miR-107 during its action on EPCs. [score:3]
Therefore, the aim of this study was to examine the expression of miR-107 in EPCs in hypoxia, and elucidate the effect and the mechanism of miR-107 on EPC differentiation. [score:3]
miR-107 is overexpressed in several tumor types, including colon, pancreas, and stomach cancers [18]. [score:3]
Then, miR-107 over-expressed EPCs and control group were induced into endothelial cells under hypoxic or normoxic conditions. [score:3]
The miR-107 was highly expressed under the hypoxic condition. [score:3]
Therefore, hypoxia promoted EPCs differentiation and increased miR-107 expression. [score:3]
Microarray -based expression profiles revealed miR-107 was induced in response to low oxygen conditions [6]. [score:3]
We found miR-107 was highly expressed under hypoxic conditions (Fig. 2d). [score:3]
Lentiviral vectors expressing miR107 (lenti miR-107), HIF-1β (lenti HIF-1β) and scrambled sequences of HIF-1β were generated. [score:3]
There has been some controversy surrounding the target of miR-107. [score:3]
Contrarily, other researchers have reported that the 3′UTR of HIF-1β contained a potential binding element for miR-107 with an 8-nt match to the miR-107 seed region, suggesting that the HIF-1β 3′UTR is a target of miR-107 [21]. [score:3]
Lentiviral supernatants were produced by expression vector pCDH-CMV-MCS-EF1-Puro-miR107 co-transfection of 293 T cells (ATCC) with psPAX2, pMD2G and either pCDH-CMV-MCS-EF1-Puro- HIF-1β and pL KO-shRNA1- HIF-1β. [score:3]
We next transfected EPCs with miR-107 inhibitor. [score:3]
To explore the biological function of miR-107, we first defined its expression in endothelial cells under hypoxic conditions. [score:3]
CD31 (d) and eNOS (e and f) expression of EPCs after infection by siRNA against lenti miR-107 and HIF-1β (#p>0.05 between groups). [score:3]
0040323.g005 Figure 5. CD31 (a) and eNOS (b and c) expression of EPCs after infection by both lenti miR-107 and lenti HIF-1β (#p>0.05 between groups). [score:3]
CD31 (a) and eNOS (b and c) expression of EPCs after infection by both lenti miR-107 and lenti HIF-1β (#p>0.05 between groups). [score:3]
d) miR-107 expression under normoxic and hypoxic conditions were detected by Q-PCR. [score:3]
miR-107 modulation of EPC differentiation may play an important role in angiogenesis because of its target, HIF-1β. [score:3]
Collectively, these findings revealed that HIF-1β is the target of miR-107 in EPCs. [score:3]
EPCs overexpression of miR-107 and HIF-1β were cultured in hypoxic or normoxic conditions for 14 days. [score:3]
Hypoxia promoted EPC differentiation and increased miR-107 expression. [score:3]
In hypoxic conditions, we found the degree of EPC differentiation exceeded that of miR-107 overexpressed EPCs. [score:3]
First, it is still unknown whether hypoxia increases miR-107 expression in EPCs via a HIF dependent mechanism. [score:3]
The present study revealed miR-107 expression increases in EPCs under hypoxic conditions. [score:3]
This result suggests that low oxygen alone induces EPC differentiation, while the addition of miR-107 partially inhibits EPC differentiation. [score:3]
To identify the HIF-1α or β dependent pathways that are involved in miR-107 mediated EPC differentiation in hypoxia, we first explored miR-107 regulation of HIF-1α or β in EPCs under both hypoxic and normoxic conditions. [score:2]
Conversely, knockdown of miR-107 in hypoxia induced EPC differentiation more than hypoxia alone. [score:2]
These researchers stated that liver and blood specific stability of HIF-1α mRNA was regulated by miR-107 [20]. [score:2]
MiR-107 suppressed the differentiation of EPCs. [score:2]
MiR-107 decreased HIF-1β expression of EPCs in normoxia and hypoxia. [score:2]
The same results occurred with knockouts of both miR-107 and HIF-1β in EPCs. [score:2]
To investigate the correlation between miR-107 and HIF-1β on EPCs differentiation, we altered their endogenous expression. [score:1]
However, miR-107 did not affect the counterpart of HIF-1β, namely HIF-1α. [score:1]
Then we explored the relationship between miR-107 and HIF-1β in both normoxic and hypoxic conditions. [score:1]
In contrast, we also transfected EPCs with two lentiviruses, one carrying siRNA against miR-107 and another carrying siRNA against HIF-1β. [score:1]
A recent study has also shown that breast cancer patients with higher miR-107 levels display a significantly better probability of metastasis-free survival [19]. [score:1]
[N: EPCs cultured under normoxic conditions; N+L: EPCs infected with both lenti miR-107 and lenti HIF-1β cultured under normoxic conditions; L: EPCs cultured under hypoxic conditions; L+L: EPCs infected with both lenti miR-107 and lenti HIF-1β cultured under hypoxic conditions. [score:1]
Both lenti-miR107 and lenti-HIF-1β were transfected into EPCs. [score:1]
Subsequently, we aimed to determine the potency and the mechanism of miR-107 or shRNA-miR-107 on EPC differentiation. [score:1]
To explore the role of miR-107 in the EPC differentiation in vitro, we altered the endogenous miR-107 in the EPCs. [score:1]
Effect of miR107 on EPCs differentiation in vitro. [score:1]
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[+] score: 235
We found that suppressed Dicer-1 expression (Fig. 5A–D, P <  0.05) in anti-miR-107 transfected HUVECs under OGD resulted in strong induction of VEGF165 expression (Fig. 5A–D, P <  0.05), confirming that, under hypoxia, miR-107 induced VEGF165 expression by suppressing Dicer-1. Upregulation of miR-107 by injecting agomir-107 into lateral ventricles resulted in increased number of capillaries in IBZ as compared with agomir control group (Fig. 6A,B, P <  0.05). [score:13]
3) miR-107 up-regulated the expression of endogenous VEGF165 in HUVECs (or endogenous VEGF164 in RBMECs) by directly downregulating the expression of Dicer-1. 4) miR-107 therapy significantly reduced the overall infarct volume following cerebral ischemia by improving angiogenesis. [score:12]
This concept was tested by transfecting HUVECs in vitro with miR-107-downregulating lentivirus (anti-miR-107) and Dicer-1-downregulating lentivirus (anti-Dicer-1) to reduce the expression of miR-107 and Dicer-1 (Fig. 5C, P <  0.05). [score:9]
These results confirmed that miR-107 suppressed Dicer-1 expression to up-regulate endogenous (ECs derived), instead of astrocyte-derived VEGF165 (VEGF164). [score:8]
In vivo, after miR-107 expression was down-regulated by lateral ventricular injection of antagomir-107 in rats brain, Dicer-1 expression was increased on day 7 after pMCAO (Fig. 4J, P <  0.05). [score:8]
To explore the molecular mechanisms involved in regulation of VEGF165/VEGF164 expression by miR-107 in endothelial cells, we examined the potential target of miR-107 using gene-chip assay (Fig. 4A), and found 96 target genes (Fig. 4B). [score:7]
control group (D) data of VEGF165 in HUVECs from over -expression of miR-107 under normoxia and down-regulation of miR-107 under OGD for 12 h (E) data of VEGF164 in RBMECs (F) data of VEGF164 in astrocytes. [score:6]
Likewise, down-regulation of miR-107 by transfection with anti-miR-107 decreased the expression of endogenous VEGF165 or VEGF164 in HUVECs and RBMECs (Fig. 3D,E, P <  0.05). [score:6]
On the other hand, the miR-107-downregulating lentiviral vector (anti-miR-107) transfected HUVECs and RBMECs expressed lower levels of miR-107 resulting in reduction of tubular length by 14.67 fold and 10.11 fold under OGD (Fig. 2A–F, P <  0.05). [score:6]
In the present study, we demonstrated that 1) miR-107 expression was significantly upregulated in the IBZ after pMCAO in rats and in ECs and astrocytes subjected to OGD for 12 h. 2) miR-107 significantly enhanced tube formation and migration of ECs resulting in increased angiogenesis both in vitro and in vivo. [score:6]
This study demonstrated that miR-107 upregulated the expression of endogenous VEGF 165 (VEGF164) via Dicer-1 under hypoxia both in vivo and in vitro. [score:6]
Under hypoxia, down-regulation of Dicer-1 could strongly induce mRNA expression of VEGF165 in anti-miR-107 -transfected HUVECs. [score:6]
To confirm that miR-107 exerts its effect on angiogenesis through down-regulation of Dicer-1, we designed a strategy (Fig. 5E) to validate the functional relevance of those downstream target genes. [score:6]
The expression of miR-107 was up-regulated by 2.21 fold and 2.88 fold (Fig. 1A,B, P <  0.05) on day 3 and day 7 respectively in the IBZ of pMCAO rats compared to control as detected by quantitative real-time PCR (qRT-PCR). [score:5]
If Dicer-1 was responsible for the effect of miR-107 on VEGF165, RNA interference with Dicer-1 expression (by lentivirus transfection) should specifically counteract the effect of anti-miR-107 in the expression of Dicer and VEGF165. [score:5]
Cells were transfected with miR-107 overexpressing lentivirus mediated (miR-107), miR-107 down -regulating lentivirus mediated (anti-miR-107), Dicer-1-down -regulating lentivirus mediated (anti-Dicer-1) or corresponding scramble versus lentivirus (scr-miR) by using lipfectamine2000TM (Invitrogen, Carlsbad, CA, USA) according to the manufacturer’s instructions. [score:5]
miR-107 regulates the expression of endogenous VEGF165 or VEGF164 via Dicer-1 by miR-107. [score:4]
We also examined the molecular mechanism by which miR-107 regulated endothelial cell-derived VEGF165 or VEGF164 expression. [score:4]
Upregulation of miR-107 strongly promoted endogenous VEGF164 and VEGF165 levels in RBMECs and HUVECs respectively (Fig. 3D,E,G). [score:4]
Dicer-1 is direct target of miR-107. [score:4]
When subjected to OGD for 12 h, which results in upregulation of miR-107, Dicer-1 dropped in both HUVECs and RBMECs whereas there was no effect in astrocytes (Fig. 4C, P <  0.05). [score:4]
These findings indicate that Dicer-1 was a direct target of miR-107. [score:4]
Regulation of the expression of endogenous VEGF165 or VEGF164 by miR-107. [score:4]
96 possible miR-107 targets were identified using gene-chip assay (Fig. 4A,B), and Dicer-1 was found to possess a specific binding site for miR-107 using miRanda 12, RNAhybrid 13 and TargetScan 14. [score:4]
miR-107 regulates the expression of endogenousVEGF165 or VEGF164 via Dicer-1. Discussion. [score:4]
In the present study, we demonstrated that, in vivo, down-regulation of miR-107 (Fig. 1E) significantly decreased the vascular density after pMCAO (Fig. 1C,D). [score:4]
Regulation of the expression of endogenousVEGF165 or VEGF164 by miR-107. [score:4]
Inhibition of miR-107 by subjecting HUVECs and RBMECs to OGD significantly reduced tubular length (Fig. 2A–F). [score:3]
However, miR-107 was found to exert limited effect on the expression of endogenous VEGF164 in astrocytes (Fig. 3F). [score:3]
Further detection showed that up-regulation of miR-107 level by lateral ventricular injection of agomir-107, a synthetic double stranded miR-107 mimics, in pMCAO rats increased the level of VEGF164 as compared with agomir control (agomir-ctl) group on day 3 and day 7 in IBZ (Fig. 3C, P <  0.05). [score:3]
showed that miR-107 level was upregulated significantly by 2.99 fold, 2.24 fold and 2.96 fold in rat brain microvascular endothelial cells (RBMECs), HUVECs and astrocytes respectively under Oxygen- Glucose Deprivation (OGD) compared with normoxia after 12 hours. [score:3]
In this study, we found that VEGF164 was increased in rat IBZ after pMCAO (Fig. 3A,B) and miR-107 promoted the expression of VEGF164 in IBZ after pMCAO (Fig. 3C). [score:3]
Left, Localization of binding sites for human miR-107 (hsa-miR-107) in the 3′UTR of target mRNA and their evolutionary conservation. [score:3]
Here, we showed that Dicer-1 was a direct target of miR-107 using dual luciferase reporter assay (Fig. 4K). [score:3]
On the other hand, transfection with anti-miR-107 in HUVECs and RBMECs increased Dicer-1 expression (Fig. 4E–I, P <  0.05) under OGD. [score:3]
To validate that Dicer-1 was the target of miR-107, HUVECs and RBMECs were transfected with miR-107. [score:3]
The mRNA expression level of VEGF164 was increased in IBZ on day 3 and day 7 after pMCAO in rats, presenting the same trend as that with miR-107 (Fig. 3A,B, P <  0.05). [score:3]
The expression pattern of HIF1α was similar to that of miR-107 (supplemental Figure S1). [score:3]
Previous studies mainly focused on the response of miR-107 to various stresses, but little is known about the functional consequences of elevated miR-107 expression in angiogenesis after stroke. [score:3]
Figure 3D,E showed that miR-107 up-regulation in HUVECs and RBMECs also raised the levels of endogenous VEGF165 or VEGF164 as compared with scr-miR. [score:3]
Notably, we found that transcription factor Dicer-1 possesses a specific binding site for miR-107 by using miRanda 12, RNAhybrid 13 and TargetScan 14. [score:3]
All of these findings strongly indicated that miR-107 regulates endothelial cell-derived VEGF165 (VEGF164) levels to promote angiogenesis. [score:2]
How to cite this article: Li, Y. et al. MicroRNA-107 contributes to post-stroke angiogenesis by targeting Dicer-1. Sci. [score:2]
Compared with the control group and negative control group (scr-miR), the relative expression of VEGF165 (in the western blot assay) was increased in the miR-107 group and decreased in the anti-miR-107 group (Fig. 3G). [score:1]
RBMECs and HUVECs transfected with miR-107, anti-miR-107 or scr-miR (10 [4]/well) and un -transfected RBMECs and HUVECs (10 [4]/well) were seeded into the upper chambers of the wells in 200 μl DMEM, and the lower chambers were filled with 500 μl ECM medium, used for inducing cell migration. [score:1]
Moreover, as a potential protector of ischemia -induced cerebral injury, miR-107 could increase the vessel density in IBZ and thereby reduce the overall infarct volume (Fig. 6A–D). [score:1]
HUVECs were transfected with miR-107 or anti-miR-107 (in parallel with control molecules miR-ctl and anti-miR-ctl). [score:1]
As a result, miR-107 improved angiogenesis and reduced overall infarct volume after ischemia. [score:1]
Similarly, invasion of HUVECs was also reduced by 58.2% following anti-miR-107 transfection under OGD at 12 hours (Fig. 2I,J, P <  0.05). [score:1]
We found that miR-107 significantly inhibited luciferase activity which is a measure of transcriptional activity (Fig. 4K, P <  0.05). [score:1]
When Dicer-1 was silenced, anti-miR-107 failed to decrease endogenous VEGF165 in HUVECs (Fig. 5A–D). [score:1]
Increased miR-107 in IBZ promotes angiogenesis in rat after pMCAO. [score:1]
Therapy with miR-107 Improves Angiogenesis after pMCAO. [score:1]
Luciferase-wt and Luciferase-mut were co -transfected with in-vitro-produced miR-107 or anti-miR-107 into HUVECs. [score:1]
Furthermore, miR-107 also promoted tubular formation and migration of RBMECs and HUVECs (Fig. 2G–L). [score:1]
HUVECs transfected with miR-107, anti-miR-107 or scr-miR and un -transfected HUVECs (5 × 10 [5] per well) were seeded into 24-well plates and allowed to adhere for 24 h. Artificial wounds were made by cutting the monolayer cells with a 200-μl pipette tip. [score:1]
miR-107 enhances tubular formation and migration of RBMECs and HUVECs in vitro. [score:1]
BMECs and HUVECs transfected with miR-107, anti-miR-107 or scr-miR (10 [4] cells/100 μl) and un -transfected RBMECs and HUVECs (10 [4] cells/100 μl) suspended in ECM were plated into a coated well, and incubated for 24 h at 37 °C. [score:1]
Bottom: Tube formation capacity of HUVECs transfected with anti-miR-107 or scr-miR and un -transfected HUVECs (sham). [score:1]
Thus, miR-107 could impair the stability of both Dicer-1 mRNA and protein (Fig. 4E–J). [score:1]
These results suggested that miR-107 promoted angiogenesis both in vivo and in vitro. [score:1]
Then, we integrated the respective 3′UTR regions of Dicer-1 into a luciferase reporter gene and determined the luciferase activity in HUVECs transfected with synthetic miR-107 precursors. [score:1]
Conversely, after down -regulating the level of miR-107 in RBMECs by transfection with anti-miR-107, we found that migration of RBMECs was impeded by approximately 70% as compared with scr-miR (negative control group) and un -transfected cells (control group) under OGD at 12 h (Fig. 2G,H, P <  0.05). [score:1]
Bottom: RBMECs transfected with anti-miR-107 or scr-miR and un -transfected RBMECs (sham) were incubated on a Transwell system under OGD. [score:1]
miR-107 enhances tubular formation and migration of RBMECs and HUVECs in vitroThe Matrigel assay demonstrated that HUVECs and RBMECs transfected with miR-107 -overexpressing lentiviral vector (miR-107 group) were found to have enhanced tubular formation, as indicated by increased number of branch points, and most prominently, by increased tubular length (by 7.98 fold and 4.39 fold, P <  0.05), as compared with negative-control scramble lentivirus transfected cells (scr-miR group; negative control group) and un -transfected cells (control group) under normoxia (Fig. 2A–F, P <  0.05). [score:1]
and had binding sites with HIF1α 5. In the present study, we further confirmed that miR-107 was strongly induced in IBZ after pMCAO (Fig. 1A,B) and in HUVECs, RBMECs and astrocytes under OGD (Fig. 1F–H). [score:1]
The relative expression of mature miR-107 was calculated against U6 RNA (internal control) by using the 2 [ΔΔCt] method. [score:1]
anti-miR-107 group. [score:1]
A previous study demonstrated that miR-107 was a member of HRMs. [score:1]
To assess the effect of miR-107, single lateral ventricular injection of antagomir-107 (12 mg/kg body weight each RIBOBIO, CHINA), agomir-107 (12 mg/kg body weight each RIBOBIO, CHINA) were given respectively. [score:1]
The samples were divided into groups: miR-107 group (or anti-miR-107 group), anti-Dicer group, scr-miR group, and un -transfected group (control). [score:1]
The miR-107, anti-miR-107, anti-Dicer-1 and the corresponding negative controls (scr-miR) were chemically synthesized by Genechem (Shanghai, China). [score:1]
The Matrigel assay demonstrated that HUVECs and RBMECs transfected with miR-107 -overexpressing lentiviral vector (miR-107 group) were found to have enhanced tubular formation, as indicated by increased number of branch points, and most prominently, by increased tubular length (by 7.98 fold and 4.39 fold, P <  0.05), as compared with negative-control scramble lentivirus transfected cells (scr-miR group; negative control group) and un -transfected cells (control group) under normoxia (Fig. 2A–F, P <  0.05). [score:1]
Overall, our findings suggest that miR-107 may serve as a valuable therapeutic entry point for improving prognosis after stroke. [score:1]
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3
[+] score: 95
Other miRNAs from this paper: rno-mir-103-2, rno-mir-103-1, rno-mir-122, rno-mir-370, rno-mir-539
In cultured hepatocytes, we observed that only those over -expressing miRNA-107-3p showed the down-regulation of CPT1a protein expression, suggesting that in fact cpt1a is a real target gene for miRNA-107-3p, but not for miRNA-103-3p. [score:10]
Finally, CPT1a protein expression was down-regulated by the over -expression of miRNA-107-3p (p < 0.001) (Figure 2). [score:8]
In the in vivo study, resveratrol induced the down-regulation of miRNA-103-3p and miRNA-107-3p in the liver, which was accompanied by a reduced expression of SREBP1. [score:6]
In our in vitro study, the over -expression of miRNA-103-3p and miRNA-107-3p in hepatocytes led to an increased expression of SREBP1, suggesting that in fact they were positive regulators. [score:6]
In our in vivo experiment, rats treated with resveratrol showed decreased miRNA-107-3p expression and increased CPT1a protein expression. [score:5]
All in all, these results suggest that the increase induced by resveratrol in CPT1a protein expression, which is involved in the liver delipidating effects of this polyphenol, was mediated by a reduction in miRNA-107-3p expression. [score:5]
In this context, the aim of the present study was to determine whether, as in the case of other polyphenols, this reduction in liver fat was mediated by changes in the expression of miRNA-122-5p, miRNA-103-3p and miRNA-107-3p, which represent more than 75% of total miRNAs in the liver [19, 21, 22, 23, 24, 25], as well as in their target genes. [score:5]
The present study provides new evidence showing that srebf1 is a target gene for miRNA-103-3p and miRNA-107-3p and cpt1a a target gene for miRNA-107-3p. [score:5]
In rats treated with resveratrol, we found a significantly decreased expression of miRNA-103-3p, miRNA-107-3p and miRNA-122-5p, which was paralleled by a significant decrease in SREBP1 protein expression. [score:5]
Furthermore, the reduction in liver steatosis induced by resveratrol under our experimental conditions is mediated, at least in part, by increased CPT1a protein expression and activity, via a decrease in miRNA-107-3p expression. [score:5]
With regard to miRNA-103-3p and miRNA-107-3p, as indicated before in the Discussion section, computational analysis (miRecords) revealed complementarity between these miRNAs and the 3′UTR region of srebf1, suggesting that it can be a direct target gene. [score:4]
Taking all that into account, it may be said that miRNA-103-3p and miRNA-107-3p are involved as positive regulators in the effects of this polyphenol on SREBP protein expression [35]. [score:4]
MiRNA-103-3p, miRNA-107-3p and miRNA-122-5p were individually over-expressed in AML12 hepatocytes. [score:3]
As far as the lipogenic pathway is concerned, miRecords data base showed that srebf1 was a predicted target gene for miRNA-103-3p and miRNA-107-3p and fasn for miRNA-122-5p. [score:3]
According to the miRecords data base, cpt1a is a predicted target gene for miRNA-103-3p and miRNA-107-3p. [score:3]
It has been reported in the literature that different types of polyphenols, such as proanthocyanidins or a mixture extracted from Hibiscus sabdariffa, are able to modify the expression of miRNA-122-5p (a liver specific miRNA and the most abundant one) and the paralogs miRNA-103-3p and miRNA-107-3p in liver [16, 17, 18, 19]. [score:3]
In addition, we reviewed the literature and found that several authors had proposed srebf1 and fasn as target genes for miR-122-5p and miR-107-3p, respectively (Table 1). [score:3]
Bhatia et al. [30] transfected HepG2 hepatocytes with miRNA-107 at various doses and they observed that, using the most common dose in transfection studies (25 nM), no changes in FAS protein expression were observed. [score:3]
In the present study, we observed that the expression of the three miRNA analysed (miRNA-103-3p, miRNA-107-3p and miRNA-122-5p) was significantly reduced in the liver of rats treated with resveratrol (Table 2). [score:3]
The targeted miRNA assay sequences were as follows (source miRBase): rno-miRNA-103-3p: 5′-AGCAGCAUUGUACAGGGCUAUGA-3′ rno-miRNA-107-3p: 5′-AGCAGCAUUGUACAGGGCUAUCA-3′ rno-miRNA-122-5p: 5′-UGGAGUGUGACAAUGGUGUUUG-3′ PCR was performed in an iCycler™–MyiQ™ Real-time PCR Detection System (Applied Biosystems, Foster City, CA, USA). [score:2]
The targeted miRNA assay sequences were as follows (source miRBase): rno-miRNA-103-3p: 5′-AGCAGCAUUGUACAGGGCUAUGA-3′ rno-miRNA-107-3p: 5′-AGCAGCAUUGUACAGGGCUAUCA-3′ rno-miRNA-122-5p: 5′-UGGAGUGUGACAAUGGUGUUUG-3′PCR was performed in an iCycler™–MyiQ™ Real-time PCR Detection System (Applied Biosystems, Foster City, CA, USA). [score:2]
Hepatocytes in a confluence status of approximately 90%, were transfected with Lipofectamine RNAiMAX (Applied Biosystems, Foster City, CA, USA) prepared following the manufacturer’s protocol, with mirVana miRNA mimics of mmu-miRNA-103-3p, mmu-miRNA-107-3p and mmu-miRNA-122-5p (homologous to rno-miRNA-103-3p, rno-miRNA-107-3p and rno-miRNA-122-5p respectively) (Applied Biosystems, Foster City, CA, USA). [score:1]
Bhatia H. Verma G. Datta M. MiR-107 orchestrates er stress induction and lipid accumulation by post-transcriptional regulation of fatty acid synthase in hepatocytesBiochim. [score:1]
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4
[+] score: 49
At 2 h, we saw a trend of upregulation of miR-29b in neurons that steadily increased up to 4-fold at 24 h. In contrast, in astrocytes, miR-29b showed a trend of upregulation later, after 6 h and a significant level increase by 2-fold only after 12 h. MiR-30b, miR-107 and miR-137 were uniquely upregulated only in astrocytes at different time-points, starting 6 h after OGD event. [score:10]
In line with our findings in cell cultures, Liu and colleagues [34] also found an increase in expression levels of miR-107 (at 24 h) in brain tissue of an intraparenchymal hemorrhage adult rat mo del, while Ren dell [35] reported a downregulation of miR-107 (at 3, 24, 72 h) in the TBI adult rat mo del. [score:6]
It can be speculated that changes in expression levels of miR-107 in astrocytes after OGD, may modulate inflammation and gliotic processes in the brain after hypoxic injury through alteration of GRN expression. [score:5]
A recent study by Wang and colleagues [75], indicated that miR-107 contributes to GRN expression regulation in human H4 neuroglioma cells and a TBI rat mo del. [score:4]
A direct comparison of expression levels of all the miRNAs used for our study between neurons and astrocytes undergoing OGD conditions, showed a significant difference at different time-points only for miR-29b, miR-30b, miR-107 and miR-137 (Figure 1). [score:4]
MiR-107, miR-30 and miR-137 were upregulated only in astrocytes. [score:4]
MiR-30b, miR-107 and miR-137 did not alter their expression levels in neurons. [score:3]
MiR-107 was upregulated 1.56-fold at 8 h and 1.7-fold at 12 and 24 h (p<0.05). [score:3]
We screened the same miRNAs as described above (miR-21, miR-29b, miR-30b, miR-107, miR-137, miR-210) and found that IGF-I significantly decreases the expression of mir-29b in neurons. [score:3]
MiR-29b, miR-30b, miR-107 and miR-137 showed a significant difference in their expression levels between neurons and astrocytes undergoing OGD conditions (Figure 1). [score:3]
IGF-I did not have an effect on the expression levels of mir-21, mir-30b, mir-107, mir-137, or mir-210 in neurons. [score:3]
We screened the same miRNAs as described above (miR-21, miR-29b, miR-30b, miR-107, miR-137, miR-210). [score:1]
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5
[+] score: 45
Recent evidence has shown that cancer cells [53] downregulate their microRNA network by targeting DICER through the overexpression of the microRNAs miR-103 and miR-107. [score:8]
Moreover, the microRNAs miR-103, miR-107, miR-133a, miR-145, mir146a and miR-98, which presented altered expression at 7 days after SCI in both Liu's study [6] and ours, demonstrated significant alterations in the expression of their targets, according to De Biase et al. [7]. [score:7]
Similarly, we analyzed proapoptotic miR-29c, which regulates p53 -mediated apoptosis [29], as well as miR-145 and miR-107, which belong to the group of 25 microRNAs whose targets were significantly enriched in the mRNA expression patterns following spinal cord injury reported by De Biase et al. (2005). [score:6]
However, this mechanism likely does not apply to the present case because miR-103 and miR-107 appear to be downregulated following injury, and previous studies have not found significant changes in DICER or DROSHA expression [7]. [score:6]
For the microRNAs that were downregulated at 3 dpo, miR-29c and miR-107 were significantly repressed in the injured animals compared only to the control group, whereas miR-219-5p was significantly downregulated in comparison to both the control and the sham groups. [score:6]
However, contrary to the current evidence, these authors observed a miR-107 upregulation 4 hours after injury, which they proposed should decrease BCL-2 levels and induce apoptosis. [score:4]
Conversely, the expression of miR-219-5p, miR-107 and miR-29c were repressed at 7 dpo. [score:3]
Specifically, miR-Let7a, miR-107, and miR-183 have been described as regulators of cell death, and miR-181b and miR199 are involved in the control of inflammation (see file S6). [score:2]
Regulation of BCL-2 by miR-107 and other microRNAs was recently discussed in a profiling study by Liu et al. [6]. [score:2]
We validated the changes in the levels of the microRNAs miR-21, miR-223, miR-146a, miR-219-5p, miR-29c, miR-468, miR-145 and miR-107 using Q-PCR. [score:1]
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6
[+] score: 45
Up-regulation of brain-enriched miR-107 promotes excitatory neurotoxicity through down-regulation of glutamate transporter-1 expression following ischaemic stroke. [score:9]
As miR-107 has been described in literature regulating GRN expression and changing in hypoxic conditions (Yang et al., 2014), we also analyzed its expression in SK-N-BE under normoxic and hypoxic conditions. [score:6]
Wang et al. (2010) described a down-regulation of this miRNA in a mouse mo del of traumatic brain injury, speculating that miR-107 plays a role in modulating neuronal repair and regeneration in the mammalian brain through molecular regulation of GRN. [score:5]
miR-107 regulates granulin/progranulin with implications for traumatic brain injury and neurodegenerative disease. [score:4]
In the middle, graphs show a negative correlation between GRN and miR-659-3p expression levels (C) and no correlation between GRN and miR-107 (D) in SK-N-BE. [score:3]
Figure 6Twenty-four hours of hypoxia treatment affect GLUT-1 and GRN transcripts and miR-659-3p and miR-107 expression in SK-N-BE cell lines. [score:3]
GRN expression is also under the post-transcriptional control of miR-107 (a member of a miRNA group also including miR-15, miR-16, miR-103, miR-195, miR-424, miR-497, miR-503, and miR-646), with implications for brain disorders (Wang et al., 2010). [score:3]
Sequence elements in the open reading frame rather than the 3′ untranslated region of GRN mRNA are recognized by miR-107 and are highly conserved among vertebrate species. [score:3]
We did not find any correlation between miR-107 and GRN mRNA expression (Figure 6D). [score:3]
A high-throughput experimental miRNA assay showed that GRN is the strongest target for miR-107 in human H4 neuroglioma cells (Wang et al., 2010). [score:2]
Figure 7 GRN mRNA, miR-659-3p and miR-107 levels in a rat mo del of global perinatal asphyxia. [score:1]
The histograms show levels of GRN mRNA (A), miR-659-3p (B) and miR-107 (C) in cortex of control and asphyctic newborn rats at different time points after global perinatal asphyxia. [score:1]
As for the in vitro analysis, we also evaluated miR-107 expression after perinatal asphyxia finding no alteration of this miRNA (Figure 7C). [score:1]
However, the analysis of miR-107 in our experimental mo dels did not show any alteration both in vitro and in vivo mo dels. [score:1]
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7
[+] score: 33
In our study, tomato up-regulated the LV expression of miR-107 and miR-486, and down-regulated the expression of miR-350 and miR-872. [score:11]
Regarding LV miRNA expression, tomato intake was significantly associated with the up-regulation of miR-107 (p = 0.043) and miR-486 (p = 0.001) and the down-regulation of miR-350 (p = 0.035) and miR-872 (p = 0.037) (Figure 3). [score:9]
Meng et al. showed that miR-107 was up-regulated in hypoxia and prevented endothelial progenitor cell differentiation via down-regulation of the transcription factor hypoxia-inducible factor (HIF)-1β [40]. [score:7]
The physiological mechanism of miR-107 in the heart has not yet been studied; however, by decreasing HIF expression, it could be used as an anti-ischemic agent [40]. [score:3]
Thus, the overexpression of miR-107 could represent another potential molecular mechanism to explain our results. [score:3]
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8
[+] score: 29
0172429.g005 Fig 5 The expression levels of miRNAs miR-107, miR-181c, miR-103, miR-101, miR-29a, miR-21 and miR-9 expression levels were down-regulated in the serum of diabetic rats and IOMe -injected rats (A). [score:8]
The expression levels of miRNAs miR-107, miR-181c, miR-103, miR-101, miR-29a, miR-21 and miR-9 expression levels were down-regulated in the serum of diabetic rats and IOMe -injected rats (A). [score:8]
In addition, miR-107 down-regulated in an early stage of AD, as it has been proven that it targets BACE1, thus regulating amyloid production as well as neurofibrillary tangles [63]. [score:7]
The expression levels of miR-107, miR-181c, miR-103, miR-101, miR-29a, miR-21 and miR-9 were significantly down regulated in the blood serum of diabetic and IOMe -injected rats (Fig 5A) whereas, the expression levels of these miRNAs are normally high. [score:6]
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9
[+] score: 14
As shown in the Venn diagram in Fig.   7, notably, 23 of the 28 upregulated miRNAs in DIO + LFD mice (mmu-miR-16, mmu-let-7i, mmu-miR-26a, mmu-miR-17, mmu-miR-107, mmu-miR-195, mmu-miR-20a, mmu-miR-25, mmu-miR-15b, mmu-miR-15a, mmu-let-7b, mmu-let-7a, mmu-let-7c, mmu-miR-103, mmu-let-7f, mmu-miR-106a, mmu-miR-106b, mmu-miR-93, mmu-miR-23b, mmu-miR-21, mmu-miR-30b, mmu-miR-221, and mmu-miR-19b) were downregulated in the DIO mice. [score:7]
Notably, 23 circulating miRNAs (mmu-miR-16, mmu-let-7i, mmu-miR-26a, mmu-miR-17, mmu-miR-107, mmu-miR-195, mmu-miR-20a, mmu-miR-25, mmu-miR-15b, mmu-miR-15a, mmu-let-7b, mmu-let-7a, mmu-let-7c, mmu-miR-103, mmu-let-7f, mmu-miR-106a, mmu-miR-106b, mmu-miR-93, mmu-miR-23b, mmu-miR-21, mmu-miR-30b, mmu-miR-221, and mmu-miR-19b) were significantly downregulated in DIO mice but upregulated in DIO + LFD mice. [score:7]
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10
[+] score: 13
The presented data indicate that, among others, the activation takes place due to the opposed expression profile of genes and their regulating microRNAs at the site of inflammation (Figure 6); while the expression of all tested mesenchymal markers (Egr1, Fgf2, Fgf7, Jak2, Notch2, Hif1 α, Zeb2, Mmp9, Lox, and Vim) was significantly induced, microRNAs regulating their expression decreased (miR-192, miR-143, miR-375, miR-30a, miR-107, miR-200b, and miR-125a). [score:9]
In contrast, the expression of miR-107, a common regulator of Notch2 and Hif1 α [23, 24], decreased in colitis -induced samples (Figure 3(f)). [score:4]
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11
[+] score: 9
Inhibition of FGF signaling through SU5402 -treated primitive streak regions of chick embryos identified up-regulation of let-7b, miR-9, miR-19b, miR-107, miR-130b, miR-148a, miR-203, and miR-218 and down-regulation of miR-29a and miR-489 (Bobbs et al. 2012). [score:9]
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12
[+] score: 9
Six of them, namely, rno-miR-107-5p, rno-miR-383-5p, rno-miR-24-1-5p, rno-mir-191b, rno-miR-196b-5p, and rno-miR-3552, were upregulated, while only rno-mir-194-1 was downregulated in the MCAO group compared with the sham group. [score:6]
H2A histone family member Z (H2afz), protein tyrosine phosphatase receptor type C (Ptprc), and serine/arginine-rich splicing factor 2 (Srsf2) were extracted as target genes of rno-miR-107-5p, rno-miR-196b-5p, and rno-miR-3552, respectively. [score:3]
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13
[+] score: 8
The upregulation of miR-107 in hypoxia condition led to EPCs differentiation inhibition by targeting HIF-1β [12]. [score:8]
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14
[+] score: 7
It has been shown that miR-29, miR-15 and miR-107 are upregulated; while miR-124, miR-34 and miR-153 are downregulated in patients with AD (Delay et al., 2012; Lau et al., 2013). [score:7]
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15
[+] score: 6
The expression of miR-122, miR-93, miR-103, miR-107, miR-206, miR-143, miR-24, and miR-106b were reduced upon treatment with Tg and Tm in H9c2 cells. [score:3]
Further we found that expression of four miRNAs (miR-20a, miR-98, miR-107 and miR-126) showed a trend similar to that observed in microarray but was not statistically significant (Figure 3). [score:3]
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16
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-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-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-127, rno-mir-129-1, 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
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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17
[+] score: 4
Cui J c-Myc-activated long non-coding RNA H19 downregulates miR-107 and promotes cell cycle progression of non-small cell lung cancerInt. [score:4]
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18
[+] 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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[+] 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-100, rno-mir-103-2, rno-mir-103-1, 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
Similarly, miR-17, miR-20a, miR-21, miR-16, miR-103, and miR-107 identified in A2B5-GalC+ cells showed overlapping expression with our OPs. [score:3]
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[+] score: 3
Specifically, some studies have focused on the roles of miRNAs in the protective effects of fish oil or omega-3 PUFAs against metabolic syndrome and found that the intake of fish oil or DHA/EPA can modify the expression of miR-30b and miR-378 [49], miR-33a and miR-122 [50], miR-107 [51], miR-192, and miR-30c [52]. [score:3]
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[+] score: 3
Chronic ethanol feeding was observed to alter the expression levels of several miRNAs during liver regeneration, including miR-34a, miR-103, miR-107, miR-122 (11) and miR-21 (12). [score:3]
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22
[+] score: 3
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-129-1, 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
Another subgroup of miRNAs displayed an opposite pattern, i. e. decreased expression during latency: miR-7a-1-3p, miR-107-3p, miR-138-5p, miR-139-3p, miR-186-5p, miR-204-5p, miR-222-3p, miR-324-3p and miR-505-3p were significantly decreased during latency (peak at 4 days after SE), then gradually returned to control levels (Fig. 2, Supplementary Fig. S2). [score:3]
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23
[+] score: 2
MiR-107 is reduced in Alzheimer's disease brain neocortex: validation study[J]. [score:2]
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24
[+] score: 1
Normalization was performed to miR-103a-3p, miR-107, miR-181a-3p, miR-181a-5p, miR24-3p, miR-451a, let-7i-5p, and miR23-3p. [score:1]
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They showed that miR-298 and miR-245 increased in the blood injected ICH mo del, and that there was a miR-107, miR-200b and miR-331-5p increment in the thrombin injection mo del [8]. [score:1]
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[+] score: 1
In a previous study, we found that miR-107 significantly increased in MCAO rats and was associated with excitotoxicity [7]. [score:1]
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[+] score: 1
Recent research showed that hypothalamus let-7, miR-148a, miR-124, miR-107 and miR-370 were confirmed to be related to EA tolerance (Cui et al., 2017). [score:1]
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MicroRNA profiling identified several miRNAs that have been previously associated with cardiac hypertrophy such as miR-214, miR-23b, miR-15b, rno-miR-26b, rno-miR-221, rno-miR-222, rno-miR-107 [59], miR-23a, miR-208, rno-miR-133b, miR-19a and mi-r133a [60]. [score:1]
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The eight circulating miRNAs, miR-29a, miR-34a, miR-375, miR-103, miR-107, miR-132, miR-142-3p and miR-144, and the two tissue-specific miRNAs, miR-199a-3p and miR-223, were identified to be significantly altered in T2D across a meta-analysis of controlled profiling studies [51]. [score:1]
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