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62 publications mentioning rno-mir-221

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-221. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 157
Other miRNAs from this paper: hsa-mir-221, hsa-mir-222, rno-mir-222
These findings complement previous studies on the role of miR-221/-222 in suppression for ICAM-1 translation, as evidenced by the fact that miR-221/-222 targeted ICAM-1 3′UTR and suppressed ICAM-1 translation [13]. [score:11]
Taken together these findings underpin the role of miR-221 in regulating expression of ICAM-1. These findings are in concordance with a similar report identifying the role of miR-221 in suppression of ICAM-1 translation [13]. [score:8]
0060170.g005 Figure 5Pre-treatment of HUVECs with the IKK2/NF-κB inhibitor SC514 (10 µM) abrogated Tat -mediated down-regulation of miR-221/-222 expression. [score:8]
Pre-treatment of HUVECs with the IKK2/NF-κB inhibitor SC514 (10 µM) abrogated Tat -mediated down-regulation of miR-221/-222 expression. [score:8]
Previous reports indicate the role of miR-221 in suppressing ICAM-1 translation and regulating IFN-γ -induced ICAM-1 expression in human cholangiocytes [13]. [score:8]
Transfection of cells with a precursor control sequence, however, did not inhibit Tat -mediated induction of ICAM-1. Having determined the role of NF-kB in Tat -induced expression of ICAM-1, we next sought to examine its role in Tat -mediated down-regulation of miR-221/-222. [score:8]
To examine whether posttranscriptional regulation by miR-221/-222 was critical for Tat -induced expression of ICAM-1, HUVECs were treated with Tat and assessed for expression of miR-221/-222 by real-time PCR. [score:6]
Recent studies suggest that ICAM-1 is a target of miR-221/-222, both of which regulate ICAM-1 expression in response to inflammatory stimuli [13], [31]. [score:6]
Having determined the role of NF-kB in Tat -induced expression of ICAM-1, we next sought to examine its role in Tat -mediated down-regulation of miR-221/-222. [score:6]
Further confirmation of the role of miR-221/-222 was carried out by overexpressing miR-221/-222, which significantly decreased Tat -induced monocyte adhesion, underpinning the role of miR-221/-222 in regulating of ICAM-1 expression with concomitant monocyte adhesion. [score:6]
Overexpression of miR-221 or miR-222 inhibits monocyte adhesion induced by Tat in HUVECs. [score:5]
Tat -induced expression of ICAM-1 in HUVECs involves miR-221/-222 suppression. [score:5]
Recent reports indicate the role of miR-221/-222 in suppressing ICAM-1 expression [13], [31]. [score:5]
Tat -induced Expression of ICAM-1 in HUVECs Involves miR-221/-222 Suppression. [score:5]
These data further corroborate that Tat -mediated suppression of miR-221/-222 is involved in expression of ICAM-1 in HUVECs and also influences monocyte adhesion. [score:5]
To manipulate the cellular functions of miR-221/-222 in HUVEC cells, we utilized an antisense approach to inhibit miR-221/-222 function and transfection of cells with miR-221/-222 precursor to increase miR-221/-222 expression. [score:5]
We have demonstrated that the downregulation of miR-221/-222 involves activation of NF-kB. [score:4]
Intriguingly, homogenates of the aorta and heart also demonstrated increased expression of ICAM-1 when assessed by real-time RT-PCR and Western blot as shown in Figs. 7B and C. Furthermore, consistent with the in vitro findings, expression of miR-221, but not miR-222, was decreased in aorta isolated from HIV Tg rats, compared with the WT rats (Fig. 7D). [score:4]
In order to determine the functional relevance of miR-221/-222-regulated expression of ICAM-1 in HUVECs, monocyte adhesion assays were performed in the presence of HUVECs transfected with miR-221/-222 precursors. [score:3]
Briefly, HUVECs were grown to 70% confluency and transfected with either anti-miR-221/-222 (antisense 2-methoxy oligonucleotide to miR-221/-222, Ambion, Austin, TX, USA) or the miR-221/-222 precursor (Ambion, Austin, TX, USA) using the lipofectamine 2000 reagent (Invitrogen, Carlsbad, CA, USA) followed by analysis of ICAM-1 expression and cell adhesion. [score:3]
Following Tat -mediated stimulation of HUVECs, there was a significant decrease in the expression levels of both miR-221/-222 in HUVECs following Tat stimulation for 12 h, as assessed by real-time PCR (Fig. 4A). [score:3]
Transfection of cells with a precursor control sequence, however, did not inhibit Tat -mediated induction of ICAM-1. (A) Effect of Tat on the miR-221/-222 by real-time RT-PCR in HUVECs after 6 h exposure to Tat. [score:3]
Cells were pretreated with SC514 for 1 h followed by additional incubation for 12 h in the presence or absence of Tat and assessed for expression of miR-221/-222 by real-time PCR analysis. [score:3]
Tat -mediated Decrease of miR-221/-222 Expression Involves NF-kB Pathway. [score:3]
Next, in order to test the role of miR-221/-222 in Tat -mediated induction of ICAM-1, HUVECs were transfected with miR-221/-222 precursors for 24 h, followed by exposure to Tat for 12 h, with subsequent assessment of ICAM-1 protein expression by Western blot. [score:3]
MiR-221/-222 Regulated Expression of ICAM-1 Plays a Role in Monocyte Adhesion. [score:3]
Tat -mediated suppression of miR-221/-222 is NF-κB -dependent. [score:3]
Total RNA was isolated, and the expression of miR-221/-222 was quantified by real-time RT-PCR. [score:3]
As shown in Fig. 4B and 4C, precursors of both miR-221/-222 significantly blocked Tat -induced ICAM-1 protein expression in HUVECs. [score:3]
Furthermore, similar to our cell culture findings there was a significant decrease in the RNA expression of miR-221 in the aortas isolated from HIV Tg rats compared with the WT controls. [score:2]
In the present study, for the first time, we report the role of Tat in modulating the regulation of ICAM-1 via miR-221/-222 in HUVECs. [score:2]
A significant decrease in miR-221/-222 levels was detected in Tat -treated HUVECs, which was significantly ameliorated in cells pretreated with SC514 (Fig. 5A, B). [score:1]
HUVECs transfected with miR-221 or miR-222 precursor or a precursor control for 24 h were exposed to Tat (14.4 nM) for 12 h followed by western blot analysis for ICAM-1. All the data are presented as mean ± SD of three independent experiments. [score:1]
The amount of miR-221/-222 was obtained by normalizing to snRNA RNU6B and relative to control as previously reported [18], [19]. [score:1]
0060170.g006 Figure 6Transfection of HUVECs with miR-221 or miR-222 precursor abrogated Tat -induced monocyte adhesion. [score:1]
0060170.g004 Figure 4(A) Effect of Tat on the miR-221/-222 by real-time RT-PCR in HUVECs after 6 h exposure to Tat. [score:1]
For analysis of miR-221/-222, total RNA was isolated from cells with Trizol reagent (Invitrogen, Carlsbad, CA, USA) according to the manufacturer’s instructions. [score:1]
Transfection of HUVECs with miR-221 or miR-222 precursor abrogated Tat -induced monocyte adhesion. [score:1]
[1 to 20 of 38 sentences]
2
[+] score: 131
Other miRNAs from this paper: rno-mir-451
Overexpression of miR-221/222 induces cell survival whereas knockdown of these miRs is accompanied by increased apoptosis by dis-inhibiting p53 upregulated modulator of apoptosis (PUMA) [24], [25]. [score:9]
MSC overexpression of miR-221 significantly enhanced cardioprotection by reducing the expression of p53 upregulated modulator of apoptosis (PUMA). [score:8]
Then, we documented: 1) significantly higher expression of miR-221/222 family in MSC than in CM; 2) enhanced cardioprotection afforded by MSC [GATA-4] and MSC [miR-221]; 3) reduction of PUMA expression in MSC by miR-221; 4) CM rapidly internalized MVs with high levels of miR-221 released from MSC; and 5) reduction of PUMA expression in CM by miR-221 transferred in MVs from MSC. [score:7]
Furthermore, overexpression of miR-221/222 increases cell survival, which is associated with the regulation of PUMA expression [24], [25]. [score:6]
miR-221 down-regulates the expression of PUMA in CM. [score:6]
We have confirmed that miR-221/222 expression in MSC is higher than in CM and that GATA-4 upregulates miR-221 in MSC. [score:6]
Expression of miR-221/222 was significantly higher in MSC than in CM and miR-221 was upregulated in MSC [GATA-4]. [score:6]
Panel B: Western blot results show that MSC-MVs highly expressed HSP70, CD63, and CD9 compared to MSC; Panel C: The expression of miR-221 in MSC-MVs, MSC, and CM analyzed using real-time PCR. [score:4]
miR-221 is known to regulate the expression of Bcl-2 family that plays an important role in cell survival. [score:4]
Overexpression of miR-221 enhances MSC mediated cardioprotection. [score:3]
Moreover, the expression of miR-221 in MSC [GATA-4] was significantly higher than that in MSC [Null] (Figure 3C). [score:3]
Moreover, we confirmed that GATA-4 can increase miR-221 expression in MSC. [score:3]
Moreover, CM co-cultured with MSC have significantly lower PUMA levels, a result that is enhanced by MSC overexpressing miR-221. [score:3]
MVs derived from MSC expressed high levels of miR-221, and were internalized quickly by CM as documented in images obtained from a Time-Lapse Imaging System. [score:3]
miR-221 transferred from MSC to CM and reduced PUMA expression in CM. [score:3]
MSC expressed green fluorescence following transfection with either lenti-miR-221 or lenti-miR-NC. [score:3]
Panel D: miR-221 expression in 293 [miR-221] and 293 [miR-NC]. [score:3]
Panel B: TargetScan shows the 3′ UTR of PUMA containing the conserved miR-221/222 binding site. [score:3]
Expression of miR-221/222 and PUMA in MSC and CM. [score:3]
Panel C: miR-221 expression in MSC [GATA-4] and MSC [Null]. [score:3]
miR-221 expression enhances MSC -mediated cardioprotection against hypoxic injury. [score:3]
The expression of miR-221/222 family in MSC was significantly higher than that in CM (Figure 3A). [score:3]
Here we have observed that overexpression of miR-221 in MSC significantly reduces CM apoptosis. [score:3]
Notably, the expression of miR-221 in MSC-MVs was significantly higher than that found in MSC (10.7-fold) or in CM (74.2-fold) (Figure 7C). [score:3]
In this study, we found that miR-221 translocation by microvesicles (MVs) plays an important role in cardioprotection mediated by GATA-4 overexpressed mesenchymal stem cells (MSC). [score:3]
0073304.g003 Figure 3Panel A: miR-221/222 expression in MSC and CM assayed using real-time PCR. [score:2]
Transfection of miR-221 into 293TN cells resulted in a significant inhibition of the basal level of the PUMA related luciferase activity compared to the cell transfected with miR-NC (Figure 3D and 3E). [score:2]
Panel A: miR-221/222 expression in MSC and CM assayed using real-time PCR. [score:2]
Lenti-miR 221-copGFP (lenti-miR-221) construct and scramble-copGFP control (lenti-miR-NC) construct were directly purchased from SBI. [score:2]
To directly detect the translocation of miRs from MSC to CM, ISH was performed after CM were co-cultured with MSC [miR-221] for 48 hours. [score:2]
Cells were then co -transfected using lipofectamine 2000 (Invitrogen) with 1 µg of lenti-miR-221, or with lenti-miR-NC and 1 µg of pEZX-MT01-PUMA. [score:1]
Moreover, CM treated with CdM [miR-221] increased MTS uptake to 73% of that in CM under normoxia, and significantly higher than that in CM treated with CdM [miR-NC] (p<0.05) (Figure 4A). [score:1]
miR-221 was observed in GFP positive MSC (green arrow) and in GFP negative cells (red arrow) (Figure 6A). [score:1]
To confirm the effect of miR-221 on 3′UTR of PUMA, transient co-transfection of lenti-miR-221 vector/or lenti-miR-NC and pEZX-MT01-PUMA in 293TN cells was performed. [score:1]
The 3′ UTR of PUMA [also recognized as Bcl-2 binding component 3 (Bbc3)] contains the conserved miR-221/222 binding sites (Figure 3B). [score:1]
miRs transfer from MSC to CM – effect of miR-221 on PUMA levels. [score:1]
miR-221 location was detected as a purple-blue signal by incubating cell cultures with NBT/BCIP. [score:1]
Panel E: PUMA in 293 [miR-221] and 293 [miR-NC], respectively. [score:1]
Panel A: In situ hybridization staining of miR-221 in CM co-cultured with MSC [miR-221] for 48 hours. [score:1]
CdM [bas]: CdM derived from MSC [bas]; CdM [miR-NC]: CdM derived from MSC [miR-NC]; and CdM [miR-221]: CdM derived from MSC [miR-221]. [score:1]
0073304.g006 Figure 6Panel A: In situ hybridization staining of miR-221 in CM co-cultured with MSC [miR-221] for 48 hours. [score:1]
We found that miR-221 was higher (1.35 fold) and PUMA protein was lower in CM co-cultured with MSC [GATA-4] than that co-cultured with MSC [Null], but without significant difference. [score:1]
miR-221 is shown as a purple-blue signal (red circles) which was observed in both GFP positive MSC (green arrow) and GFP negative CM (red arrow). [score:1]
ISH was performed using a double-digoxigenin (DIG)-labeled miRCURY LNA miR detection probe against has-miR-221 (EXIQON) and IsHyb-ISH Kit according to manufacturer's instructions (BioChain). [score:1]
Our studies indicate that MSC [GATA-4] mediated cardioprotection is conferred, at least in part, by miR-221 carried in MVs. [score:1]
293 [miR-NC] = 293TN transfected with lenti-miR-NC; 293 [miR-221] = 293TN transfected with lenti-miR-221; MSC [bas] =  basal MSC; MSC [miR-221] = MSC transfected with miR-221; MSC [miR-NC] = MSC transfected with miR-NC. [score:1]
CdM [miR-221] showed a more powerful potential in preventing caspase 3/7 activation induced by hypoxia comparing with CdM [miR-NC] (Figure 4B). [score:1]
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3
[+] score: 99
Other miRNAs from this paper: rno-mir-222
We found that SOCS1 overexpression in BRL cells reduces Met expression (Fig.   3D) and induces a dramatic decrease in miR-221 and miR-222 expression (Fig.   3E). [score:7]
In vivo, we used Pearson’s correlation analysis to analyze the potential correlation between miR-221/222 expression and SOCS1 mRNA expression in liver tissue. [score:5]
Although recent studies reported that miR-221/222 are involved in liver diseases, including liver fibrosis and tumorigenesis 22, 23, their potential function during cholestasis diseases, such as AOC, is unclear. [score:5]
This suggests that miR-221/222 expression in the liver may represent that of SOCS1 and indirectly reflect AOC prognosis. [score:4]
Consistent with previous studies, our results suggest that circulating miR-221/222 could reflect SOCS1 expression levels in the liver and indirectly predict the prognosis of patients with AOC. [score:4]
To confirm that miR-221/222 expression can also be regulated by SOCS1/Met axis in hepatocytes, we performed an experiment in vitro. [score:4]
Because Met activation by growth factors can enhance miR-221 and miR-222 expression, we investigated the possibility that indirectly evaluation of SOCS1 expression levels by examining miR-221 and miR-222 expression may predict AOC patient prognosis. [score:4]
As expected, SOCS1 RNA interference knockdown in rat hepatocytes showed a prominent increase of miR-221 and miR-222 expression (Fig.   3F). [score:4]
Thus, we examined miR-221 and miR-222 expression in our study. [score:3]
Our study showed that miR-221/222 expression was modulated by the SOCS1/Met axis in vitro, and confirmed the inverse correlation between SOCS1 and miR-221/222 in vivo. [score:3]
Previous studies reported that Met is able to enhance miR-221 and miR-222 expression 17, 21. [score:3]
Furthermore, Pearson’s correlation analysis also showed that miR-221 and miR-222 in serum had an inverse correlation with SOCS1 expression, which is similar to the results in liver tissue. [score:3]
miR-221/222 were reported to promote proliferation and migration by targeting SOCS1 in basal-like breast cancer [18]. [score:3]
The results suggested that lower expression of circulating miR-221 and miR-222 after ENBD was associated with delayed restoration of liver function. [score:3]
SOCS1/Met axis modulates miR-221/222 expression in hepatocytes. [score:3]
However, SOCS1 expression in BRL cells did not show the expected significant decrease after transfection with miR-221 or miR-222 (Fig.   4E), which may be because of LPS stimulation or the difference between human SOCS1 and rat SOCS1. [score:3]
Circulating miR-221 and miR-222, which are indirectly regulated by SOCS1, may be potential serological biomarkers for predicting the outcome for patients with acute obstructive cholangitis. [score:3]
The expression levels of miR-221/222 were normalized to U6 RNA (tissue samples) and spiked C. elegans miR-39 mimic (serum samples) [43]. [score:3]
We found that circulating miR-221 and miR-222 levels also were inversely correlated with SOCS1 expression in the liver (R = −0.606 and −0.512, respectively; Fig.   4A and B). [score:3]
Additionally, miR-221/222 expression can be enhanced by the activation of Met, which is a key growth factor receptor in cells 17, 21. [score:3]
More interestingly, miR-221 overexpression has been reported to accelerate hepatocyte proliferation during liver regeneration [41]. [score:3]
miR-221/222 expression is aberrant in the liver and is associated with acute obstructive cholangitis prognosis. [score:3]
miR-221/222, which can be regulated by Met [17], were suggested as possible candidates. [score:2]
Hence, miR-221/222 were more likely negatively regulated by SOCS1 during the process of AOC. [score:2]
We also investigated whether miR-221/222 reduced LPS -induced SOCS1 upregulation in hepatocytes. [score:2]
Figure 4Circulating miR-221 and miR-222 are potential biomarkers to predict acute obstructive cholangitis prognosis. [score:1]
We examined miR-221/222 levels in the serum collected 6 hours after ENBD. [score:1]
Circulating miR-221 and miR-222 are potential biomarkers to predict acute obstructive cholangitis prognosis. [score:1]
This suggests that circulating miR-221 and miR-222 are potential biomarkers to predict the AOC prognosis in the rat. [score:1]
Other RNA oligonucleotides (including miR-221, anti-miR-221, miR-222, anti-miR-222, miR control and siRNA control) was also obtained from RiboBio. [score:1]
Interestingly, comparing the results between two groups, both miR-221 and miR-222 in the bad recovery group were significantly lower than those in the good recovery group (Fig.   4D). [score:1]
A recent study verified that patients with spontaneous recovery from acute liver failure had significantly higher serum miR-221 levels than patients who did not recover [40]. [score:1]
We also examined miR-221/222 levels after BD in liver tissue from AOC rats. [score:1]
Similar to miR-221/222 in liver tissues, circulating miR-221/222 in rats with BD that survived was also higher than in rats that died or without BD (Fig.   4C). [score:1]
Both miR-221 and miR-222 had a statistically significant inverse correlation with SOCS1 (R = −0.687 and −0.632, respectively; Fig.   3G and H). [score:1]
This indicates that circulating miR-221 and miR-222 levels are associated with AOC prognosis in rats and in humans. [score:1]
Circulating miRNA is easy to detect, and we examined circulating miR-221 and miR-222 levels in rat serum. [score:1]
At 6 h after operation, we found that miR-221 increased significantly because of the obstructed biliary tract (BDL group), while there was a mild decrease in response to LPS infusion (AOC group) (Fig.   3B). [score:1]
Given that both miR-221 and miR-222 have the same sequences in humans and rats, we also explored the potential correlation between circulating miR-221/222 and prognosis of AOC patients. [score:1]
[1 to 20 of 39 sentences]
4
[+] score: 98
Other miRNAs from this paper: hsa-mir-221
Here we show that p53 up-regulation in Notch3 silenced cells is first mediated by Cyclin G1 down-regulation and than sustained by decreased level of MDM2 due to miR-221 up-regulation by p53. [score:10]
Moreover p53 silencing in Notch3 depleted cells resulted in miR-221 down-regulation and MDM2 up-regulation and (Fig. 2D-F). [score:7]
This prompted us to investigate miR-221 expression in Notch3 depleted cells and we found that it was up-regulated in HepG2 and SNU398 and down-regulated in Hep3B (Fig. 2C). [score:7]
P53 accumulation in Notch3 depleted cells triggers the up-regulation of its known transcriptional target miR-221 leading to MDM2 reduction and thus to the increased p53 stability. [score:6]
Fornari et al. recently demonstrated that p53 triggers miR-221 transcription by binding its upstream region and that miR-221 up-regulation by p53 exerts a positive feed back loop by targeting MDM2 [15]. [score:6]
As described above the knockdown of Notch3 in Hep3B cells reduced miR-221 expression leading us to hypothesize that a Notch3 target genes might affect miR-221 transcription. [score:6]
Blue panel: increased in p53 protein expression is triggered by Cyclin G1 and sustained by the miR-221-MDM2 axis in p53 wild Type HCC cells upon Notch3 inhibition. [score:5]
Figure 8 Blue panel: increased in p53 protein expression is triggered by Cyclin G1 and sustained by the miR-221-MDM2 axis in p53 wild Type HCC cells upon Notch3 inhibition. [score:5]
MDM2 protein expression is regulated by miR-221 in Notch3 depleted cells. [score:4]
Hes1 regulates miR221 expression. [score:4]
Based on this observation we analyzed miR-221 and Hes1 protein expression in cases with mutated p53 and a positive correlation was found (Spearman ρ= 0.709, p<0.05). [score:3]
To assess to what extent our in-vitro findings are representative of what occurs in human HCC, we analyzed the expression of Notch3, Hes1, Cyclin G1 and MDM2 proteins and miR-221 in 27 surgically resected HCCs by western blot and respectively (Supplemental Table 1-2). [score:3]
As it was previously proven in normal chondrocytes and in HCC cell lines MDM2 is a predicted target of miR-221 [14, 15]. [score:3]
Spearman's correlation was used to explore the relationships between Notch3 and p53 or miR-221 and Hes1 expression in HCC tissues. [score:3]
Hes1 silencing with specific shRNAs, by stable retroviral transduction (Fig. 3B) determined a reduction of miR-221 expression and increased levels of MDM2 (Fig. 3B-C). [score:3]
Notch3 controls MDM2 protein expression through miR221. [score:3]
The mechanisms herein described suggest that p53 increase consequent to Notch3 knockdown is sustained but not triggered by the p53-miR221 positive feedback loop. [score:2]
Indeed, we proved that both Hes1 and p53 are involved in miR-221 regulation. [score:2]
Finally, no correlation was found between Notch3 and miR-221 and between MDM2 and miR-221 in our human HCCs setting, supporting the hypothesis, that miR-221 is not the only actor in MDM2 regulation in vivo. [score:2]
These results collectively show that Hes1 induces the transcription of miR-221 via direct binding to its promoter region. [score:2]
Contrary in Hep3B TP53−/− cells reduced levels of miR-221, in the absence of Notch3 protein, are associated to reduced levels of Hes1 which regulates miR-221 transcription. [score:2]
HES1 binds to miR-221 promoter. [score:1]
In HepG2 cells DNA of the miR-221 promoter region could be specifically detected in the Hes1-immunoprecipitated DNA complex from formaldehyde -treated cells, indicating Hes1 occupancy at the miR-221 promoter (Fig. 3A). [score:1]
C) of miR-221 in Notch3 silenced cells. [score:1]
A bioinformatic analysis was executed in a region spanning −2500 + 1100 bp considering +1 the first nucleotide of miR-221 precursor. [score:1]
C) of miR-221 in Hes1 silenced cells. [score:1]
As expected, no significant correlation was found between Hes1 and miR-221 in the whole HCCs setting. [score:1]
F) of miR-221 in HepG2 Notch3 silenced cells transfected with p53 siRNA or scrambled RNA. [score:1]
This observation let us to hypothesize that the high levels of p53 observed in Notch3 depleted cells could increase miR-221 that, in turn, decreases MDM2 levels. [score:1]
These findings let us hypothesize the contribution of p53/miR-221 axis to MDM2. [score:1]
Taken together, our results suggest that the dominant effect on miR-221 transcription is p53 dependent. [score:1]
[1 to 20 of 31 sentences]
5
[+] score: 49
Other miRNAs from this paper: rno-mir-31a, rno-mir-187
The presented data show that upregulation of HO-1 expression resulting from the inhibition of individual miRNAs predicted to target HO-1 mRNA (i. e. rno-miR-221-3p, -221-5p, -222-3p or -326-3p), is able to trigger HO-1 dependent growth inhibition in cultured rat astrocytes. [score:12]
Using miQPCR, we confirmed the significant downregulation of 4 out of 6 miRNAs predicted to target HO-1 mRNAs, while a strong tendency towards downregulation was found for rno-miR-221-5p and -365-3p, however without reaching statistical significance (Fig. 2A). [score:9]
Indeed, hypoosmotic astrocyte swelling significantly downregulated the expression of two miRNAs predicted to target HO-1 (e. g. rno-miR-221-5p and -326-3p; Suppl. [score:8]
Cultured rat astrocytes were transfected with either miRNA inhibitors targeting rno-miR-221-3p, rno-221-5p, 222-3p or -326-3p or without inhibitor (control) and DNA content was quantified 48 h after seeding of the cells by fluorimetric detection of Hoechst34580 fluorescence as described in materials and methods. [score:7]
Importantly, proliferation inhibition by miRNA -inhibitors rno-miR-221-3p, -221-5p, -222-3p or -326-3p was prevented by SnPP, suggesting a role of HO-1 for miRNA -dependent anti-proliferative effects (Fig. 4B). [score:5]
Fig. 9B) or by inhibition of rno-miR-221-3p, -221-5p, -222-3p or -326-3p (Fig. 3A,B) impairs astrocyte proliferation (Figs 4 and 6; Suppl. [score:3]
As shown in Fig. 4A, inhibition of miR-221-3p, -221-5p, -222-3p or -326-3p significantly impaired proliferation of cultured rat astrocytes 48 h after seeding. [score:3]
By using RNA22 we additionally found 4 predicted binding sites in the HO-1 mRNA sequence for rno-miR-221-5p, which also became donwregulated by NH [4]Cl (5 mmol/l, 48 h) in cultured astrocytes (Fig. 1C, Suppl. [score:2]
[1 to 20 of 8 sentences]
6
[+] score: 33
Other miRNAs from this paper: hsa-mir-221, mmu-mir-221
Analysis of the expression of miRNA-221&222 in RNFwt and RNFmut cells, as well as in a series of normal and tumor rat adrenal tissues (organ affected by the MENX syndrome), showed no significant difference in the expression of these two miRNAs between samples expressing wild-type or mutant Cdkn1b (see Additional File 7). [score:7]
Therefore, a higher expression of miRNA-221&222 does not play a role in the low level of expression of p27fs177 in either rat primary cells or rat tissues. [score:5]
Overexpression of the negative regulators microRNA-221/222 plays no role in regulating the amount of p27fs177 in RNFs and rat tissues. [score:5]
Recently, it has been reported that miRNA-221&222 down-regulate p27 at the post-transcriptional level in cell lines and in primary tumors [8, 25]. [score:4]
Therefore, we checked whether the low amount of p27fs177 in MENX-affected rat tissues and cells might also be due to an up-regulation of miRNA-221&222. [score:4]
Expression of miRNA-221& 222 in rat adrenal tissues and in primary fibroblasts (REF cells) show no difference between normal and mutated rats. [score:3]
Click here for file Expression of miRNA-221& 222 in rat adrenal tissues and in primary fibroblasts (REF cells) show no difference between normal and mutated rats. [score:3]
Quantitation of mature miRNA-221 and 222 expression levels in and was performed by RT-PCR using TaqMan MicroRNA Assays. [score:2]
[1 to 20 of 8 sentences]
7
[+] score: 30
Other miRNAs from this paper: rno-mir-486
Since PTEN is a target of both of these microRNAs, and miR-221 was 1.5-fold down-regulated, and miR-486 was 3.15-fold up-regulated, PTEN expression in the stroked kidneys was slightly down-regulated as compared to the control kidneys. [score:13]
This protein is targeted by both miR-221 and miR-486, which exhibit opposite expression tendencies: miR-221 is down-regulated and miR-486 is unregulated in the kidney tissue of stroked animals compared with the control ones. [score:8]
miR-221 was shown to target and control expression of several key proteins such as p27 [42- 43], phosphatase, tensin homolog (PTEN) [44], Kit oncogene, and others. [score:5]
Altered expression of miR-221 and miR-486 was independently confirmed by quantitative real-time PCR analysis (Figure 5B). [score:3]
Specifically, we noted a significant decrease in the levels of miR-221 and a significant increase in the levels of miR-486 and miR-714 (p<0.05) (Figure 5A). [score:1]
[1 to 20 of 5 sentences]
8
[+] score: 27
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-31, hsa-mir-96, hsa-mir-99a, hsa-mir-16-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-182, hsa-mir-183, hsa-mir-211, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-184, hsa-mir-190a, hsa-mir-195, rno-mir-322-1, rno-let-7d, rno-mir-335, rno-mir-342, rno-mir-135b, hsa-mir-30c-1, hsa-mir-299, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, hsa-mir-382, hsa-mir-342, hsa-mir-135b, hsa-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-15b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-26a, rno-mir-26b, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-96, rno-mir-99a, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-132, rno-mir-143, rno-mir-145, rno-mir-183, rno-mir-184, rno-mir-190a-1, rno-mir-191a, rno-mir-195, rno-mir-211, rno-mir-217, rno-mir-218a-2, rno-mir-218a-1, rno-mir-222, rno-mir-299a, hsa-mir-384, hsa-mir-20b, hsa-mir-409, hsa-mir-412, hsa-mir-489, hsa-mir-494, rno-mir-489, rno-mir-412, rno-mir-543, rno-mir-542-1, rno-mir-379, rno-mir-494, rno-mir-382, rno-mir-409a, rno-mir-20b, hsa-mir-542, hsa-mir-770, hsa-mir-190b, hsa-mir-543, rno-mir-466c, rno-mir-17-2, rno-mir-182, rno-mir-190b, rno-mir-384, rno-mir-673, rno-mir-674, rno-mir-770, rno-mir-31b, rno-mir-191b, rno-mir-299b, rno-mir-218b, rno-mir-126b, rno-mir-409b, rno-let-7g, rno-mir-190a-2, rno-mir-322-2, rno-mir-542-2, rno-mir-542-3
In addition to miR-221/222, several studies also highlighted the differential regulation of let-7d, let-7f, miR-25 and miR-26b in prostate and breast cancer, as well as in leukemia by the estrogen receptor pathways and that their expression was up-regulated in ERα -positive cells [50- 52]. [score:7]
In breast cancer cells, over -expression of miR-221, miR-222, let-7 and miR-20b is associated with reduced of ERα protein content, signaling and expression of ERα target genes [47- 49]. [score:7]
Ovarian follicle expression of miR-221 and miR-222 has been reported to be repressed by androgens [42- 44] which regulates cell proliferation by targeting p27/kip1 [44, 45]. [score:6]
A list of differentially expressed miRNAs (Fold change ≥ 2 and their corresponding P value) is presented in Figure  4. Beside this group, miRNAs which were also highly abundant in DHT -treated ovaries are rno-miR-221, rno-miR-222, rno-miR-25, rno-miR-26b, rno-miR-379*, rno-let-7d, rno-miR-24, rno-miR-673, rno-miR-26b, rno-miR-335, rno-miR-382*, rno-miR-412, rno-miR-99a*, rno-miR-543, rno-miR-674-3p, rno-miR-409-3p. [score:3]
Among the fourteen miRNAs mapped to the ingenuity databases, twelve (rno-let-7d, rno-miR-132, rno-miR-182, rno-miR-183, rno-miR-184, rno-miR-21, rno-miR-221, rno-miR-24, rno-miR-25, rno-miR-26b, rno-miR-31 and rno-miR-96) had 171 experimentally validated targets. [score:3]
These include rno-miR-195, rno-miR-125a-5p, rno-let-7a, rno-miR-16, rno-miR-30b-5p, rno-let-7c, rno-let-7b, rno-miR-125b-5p, rno-miR-221, rno-miR-222, rno-miR-26a, rno-miR-322, rno-miR-23a, rno-miR-191, rno-miR-30 family, rno-miR-21, rno-miR-126, rno-miR-23b, rno-miR-145 and rno-miR-494. [score:1]
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9
[+] score: 26
Other miRNAs from this paper: rno-mir-32
We think that down-regulation of miR-221 and/or miR-32 might participate in trehalose -induced apoptosis inhibition, autophagy induction and p38 MAPK inactivation in cryoprotected rat valve cells. [score:6]
Additionally, miR-221 expression was significantly and positively correlated with cleaved caspase-3 levels; no significant relevance was observed between miR-221 expression and LC3A/B II/I ratio or p38 MAPK phosphorylation. [score:5]
Interestingly, we found that miR-221 and miR-32, which were confirmed to regulate p38 MAPK signaling in past reports, were down-regulated in the trehalose group compared to those in the DMSO group. [score:4]
Expression levels of miR-32 and miR-221 in cryopreserved valve cells. [score:3]
miR-221 may participate in trehalose -induced apoptosis inhibition in cryoprotected rat valve cells. [score:3]
However, the mechanism by which trehalose down-regulates miR-221 and miR-32 is not clear and needs further investigation. [score:2]
Thus, miR-32 and miR-221 can also act as biomarkers for assessment of the effect of cryopreservation on valves. [score:1]
The results showed that miR-221 and miR-32, which were confirmed to regulate p38 MAPK signaling in prior reports, were decreased in the trehalose group compared with the levels in the DMSO group (Fig 5). [score:1]
Additionally, miR-221 and miR-32 might participate in this reaction; these mechanisms need further studies. [score:1]
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10
[+] score: 25
In vitro overexpression of miR-221 alone is sufficient to increase the size of cardiomyocytes, accompanied by enhanced expression levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) (Wang et al., 2012). [score:5]
Upregulation of miRNA-221 is also related to antiapoptotic effects in cancer cells (Zhou et al., 2016) and showed pro-proliferative, pro-migration, and antiapoptotic effects in vascular smooth muscle cells (Zhou et al., 2016). [score:4]
The miRNA-221 is significantly upregulated in patients with hypertrophic cardiomyopathy (HCM) and in a mouse mo del of cardiac hypertrophy and heart failure induced by pressure overload (Su et al., 2015). [score:4]
In our occlusion protocol, we observed an enhanced expression of miR-221. [score:3]
The data show that mir-221 presented a method-specific switch in expression; occlusion had higher levels of these miRNAs than ablation. [score:3]
MiR-221 promotes cardiac hypertrophy in vitro through the modulation of p27 expression. [score:2]
MicroRNA-221 inhibits autophagy and promotes heart failure by modulating the p27/CDK2/mTOR axis. [score:2]
However, the in vivo roles and molecular mechanisms of miR-221 in the regulation of cardiac remo deling remain unclear. [score:2]
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11
[+] 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]
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]
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]
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12
[+] score: 21
Of the 30 miRNAs they found upregulated in traumatic spinal cord injury, miR-223, miR-214, miR-20b-5p, miR-17, miR-146a, miR-199a-3p, miR-221-3p, miR-146b, and miR-145 were also upregulated in our study, and among the 16 downregulated miRNAs in traumatic spinal cord injury, miR-34a and miR-338 were also downregulated after ventral combined with dorsal root avulsion in our study. [score:13]
We found that miR-21 and miR-221 were upregulated in the ipsilateral ventral horn after ventral combined with dorsal root avulsion. [score:4]
This result is consistent with the study by Bin Yu et al., who showed that miR-21 and miR-221 were upregulated in the dorsal root ganglia after resection of the sciatic nerve in rats [30]. [score:4]
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13
[+] score: 19
miR-221 and miR-96 showed relatively larger sex differences over the middle portion of the life span, with miR-221 expressed at 3-to 14.3-fold higher levels in males than females from 8 to 21 weeks of age, and miR-96 expressed at 2.2 to 7.2 higher levels in males than females from 21 to 78 weeks of age. [score:5]
Four of these miRNAs exhibited female-biased expression, and two exhibited male biased expression (miR-92a and miR-221). [score:5]
miR-221 showed male-biased expression at 8, 15, and 21 weeks of age, exhibiting a 14-fold difference in expression (21 weeks) compared to females. [score:4]
miRNAs showing the most male-biased expression included miR-125b-5p, miR-99a*, miR-99a, miR-96, miR-221, and miR-183 (Fig.   3). [score:3]
Among the 65 sex-biased DEMs, only 6 (miR-92a, miR-221, miR-374, miR-505*, miR-532-3p, and miR-652) are encoded on the X-chromosome. [score:1]
miR-125b-5p and miR-221 play a role in glioma carcinogenesis and have been recently proposed as prognostic markers in assessing glioma tumors [63]. [score:1]
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14
[+] score: 19
As such, the translational regulation of ESR1 represents another remarkable functional cross-talk between miRNAs, which we show to be expressed in a mutually exclusive manner between the cerebellum (miR-206) and the hippocampus/amygdaloid regions (miR-221/miR-222). [score:6]
Our data provides a detailed map of miRNA brain expression in rats and shows that there are some differences in the expression in the cerebellum of a subset of the detectable transcripts, which are either highly enriched (miR-206 and miR-497) or nearly depleted (miR-132, miR-212, miR-221 and miR-222). [score:5]
Notably, we found reciprocal expression profiles for a subset of the miRNAs predominantly found (> ten times) in either the cerebellum (miR-206 and miR-497) or the forebrain regions (miR-132, miR-212, miR-221 and miR-222). [score:3]
Accumulations of miR-497 in the cerebellum, of miR-7 in the hypothalamus, and of miR-221 and miR-222 in the hippocampus have also been described in mice [39] and zebrafish (larval and adult brain), where miR-222 is expressed in specific groups of differentiating cells in the rostral parts of the brain [42]. [score:3]
The most pronounced differences in expression patterns among these nine miRNAs were seen for the miR-221 family members (miR-221 and miR-222), which showed a cerebellar reduction of more than 60-fold compared to the hippocampus and the amygdaloid region. [score:2]
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[+] score: 16
The most relevant pathway related to the targets of miR-221-3p was cancer-related. [score:3]
Although the most relevant pathway of the targets of miR-221-3p was cancer, it was also related to the γ-aminobutyric acid (GABA) receptor, which is thought to be important in vestibular compensation [3]. [score:3]
In the miR-221-3p group, recovery of the rotarod scores was inhibited but neurogenesis did not decrease. [score:3]
Therefore, miR-221-3p may also regulate vestibular compensation. [score:2]
Therefore, we believe that the mechanisms through which miR-218a-5p and 219a-5p affect vestibular compensation involve neurogenesis in the MVN, while miR-221-3p appears to be unrelated to neurogenesis. [score:1]
Artificial cerebrospinal fluid, miR-218a-5p antagomir, miR-219a-5p antagomir, or miR-221-3p agomir were administered into the intracerebroventricular space continuously for 1 week using the brain infusion cannula. [score:1]
In the animals in which the miRNA-221-3p agomir (e) was administered, several BrdU -positive cells were observed in the MVN. [score:1]
Thirty-six rats were randomly divided into four groups: the control group (n = 9), which received artificial cerebrospinal fluid (aCSF) containing (mm): 124 NaCl, 5 KCl, 1.2 KH [2]PO [4], 1.3 MgSO [4], 2.4 CaCl [2], 26 NaHCO [3] and 10 d-glucose; the 218a-5p group (n = 9), which received the miR-218a-5p antagomir (Qiagen, Hilden, Germany); the 219a-5p group (n = 9), which received the miR-219a-5p antagomir (Qiagen); and the 221-3p group (n = 9), which received the miR-221-3p agomir (Qiagen). [score:1]
In the case of miR-221-3p, agomirs were administered. [score:1]
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16
[+] score: 16
Other miRNAs from this paper: rno-mir-222
Recently, it became apparent that microRNAs, especially miRNA-221 and miRNA-222, may be important inhibitors of Kip1 translation (Galardi et al., 2007; Martínez-Sánchez and Gebauer, 2010). [score:5]
miR-221 and miR-222 expression affects the proliferation potential of human prostate carcinoma cell lines by targeting p27Kip1. [score:5]
Data are expressed as ΔΔCt values for miRNA221 (A) or miRNA222 (B) using 4.5 S -RNA (diamonds), U6-snRNA (squares), or β-actin mRNA (full circles) as internal standards. [score:3]
We could, however, not find any obvious changes in miRNA-221 or miRNA-222 in residual liver tissue over the entire experimental period (Figure 7) indicating that these microRNAs do not contribute to the regulation of Kip1 abundance in residual liver tissue upon PH. [score:2]
Figure 7 Abundances of miRNA221 or miRNA222 in total RNA preparations from rat liver during or at different times after partial hepatectomy as determined by qPCR. [score:1]
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17
[+] score: 15
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]
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]
Some of the circulating miRNAs identified in this study have also been reported in the adipose tissue of DIO mice or implicated in adipogenic processes [11– 13], including Let-7, miR-103, miR-15, the miR-17-92 cluster (miR-17, miR-20a, and miR-92a), miR-21, miR-221, and miR-30b. [score:1]
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18
[+] score: 14
For liver cancer, one recent study reported that miR-21, miR-31, miR-122, miR-221, miR-222 were significantly up-regulated in HCC tissues, whereas miR-145, miR-146a, miR-200c, and miR-223 were found to be down-regulated [15]. [score:7]
For instance, some miRNAs, such as miR-29, miR-21 and miR-221, has been reported to regulate tumor cell growth, apoptosis, migration and invasion by targeting proteins involved in those cellular pathways [7- 9]. [score:4]
However, authors concluded that high level of miR-21, miR-31, miR-122, and miR-221 expression was correlated with cirrhosis but only miR-21 and miR-221 were associated with tumor stage. [score:3]
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[+] score: 11
On the contrary, other microRNAs identified by these authors, such as miR-152, miR-214, miR-206, and miR-221, either did not show significant expression changes or showed opposite behaviors in our analyses (such as the downregulation of miR-1). [score:6]
Expression changes respect to control/sham 1 dpo 7 dpo Name Liu Present Liu Present rno-miR-130b 1.42 NE rno-miR-146a 1.72 INC S rno-miR-15b 1.15 DEC NS rno-miR-17 1.74 INC NS rno-miR-18a 2.71 NE 3.41 NE rno-miR-200c 4.12 NE rno-miR-206 3.26 NE rno-miR-20a 1.69 NC rno-miR-20b-5p 1.83 NE rno-miR-21 1.37 INC S rno-miR-214 2.01 INC NS rno-miR-219-5p −1.82 DEC S rno-miR-221 1.1 NE rno-miR-223 3.58 INC S 3.4 INC S rno-miR-24-2* 2.41 DEC NS rno-miR-290 3.66 INC NS 2.96 DEC S rno-miR-378 1.31 INC NS rno-miR-410 −1.21 NE rno-miR-466b 3.05 DEC S rno-miR-541 1.11 INC S rno-miR-874 2,8 NEData restricted to microRNAs with significant changes in expression (2-fold or greater) according to Liu et al. [6]. [score:5]
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20
[+] score: 11
Similarly, miR-29a, miR-221 and miR-23b in this network seem to regulate the expression of Vimentin and SLUG indirectly through Caspase 7, AP-1 (activator protein 1) and PAK (p21 protein activated kinase 2). [score:5]
However, in normal human umbilical vein endothelial cells, miR-221 has been shown to directly target and repress Zeb2 [33]. [score:4]
miR-221 has been shown to be involved in the promotion of epithelial-mesenchymal transition (EMT) in breast cancer cell lines, where it is regulated by Slug [32]. [score:2]
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21
[+] score: 10
Other miRNAs from this paper: rno-mir-219a-1, rno-mir-219a-2, rno-mir-219b
MicroRNA-221/222 (miR-221/222) are also highly expressed in ECs, and one of their target genes is the cyclin -dependent kinase inhibitor, p57/Kip2 (Cdkn1c) [42]. [score:7]
So there is another possibility that miR-221/222 contained in MVEC-EVs reduces expression of p57/Kip2 in OPCs and thereby promotes OPC proliferation. [score:3]
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22
[+] score: 10
Other miRNAs from this paper: hsa-mir-221
Different expression levels of the target genes of miR-221/222 in SMCs and ECs might account for differential cellular effects of miR221/222 in these two cell types. [score:5]
For example, the oligo inhibitors of miRNA-221/222 have been reported to inhibit rat aortic SMC proliferation but stimulate human umbilical vein endothelial cell (HUVEC) growth [18]. [score:5]
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23
[+] score: 9
MiRNA-221 and miRNA-222 were upregulated in the activated astrocytes. [score:4]
MiRNA-221 was upregulated in the human astrocytic tumors [47]. [score:3]
MiRNA-221 and miRNA-222 are two highly homologous miRNAs, whose dysregulations have been recently described in several types of human tumors. [score:2]
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24
[+] score: 9
Similarly, TargetScan analysis identified the following miRNAs that are conserved in humans and are predicted to influence the NT3 gene: miR-21-5p, miR-222-3p, and miR-221-3p. [score:3]
Both miR-222-3p and miR-221-3p share the same seed sequence (AUGUAGCA). [score:1]
MicroRNAs predicted to influence neurotrophins: a BDNF (miR-206-3p, miR-10a-5p, miR-1b, miR-195-5p and miR-497-5p), b NT3 (miR-21-5p, miR-222-3p and miR-221-3p), and c NGF (let-7b-5p and miR-98-5p) were quantified by qPCR analysis in YA (n = 8) vs VO (n = 10) rat vastus lateralis muscle and WT (n = 8) vs Sarco (n = 7) gastrocnemius muscle. [score:1]
In contrast to the aforementioned studies in aging muscle, most of the miRNAs studied herein have been examined in the context of experimental denervation, including miR-206 (increases after reinnervation), miR-10a-5p (increases four- to seven-fold with denervation), miR-1 (increases up to 10-fold following denervation and remains elevated after reinnervation), miR-195 (increases up to 10-fold with denervation), miR-21 (increases with denervation), miR-221 (no consistent change), miR-222 (no consistent change), and miR-98 (increases up to 10-fold with denervation) [43, 47, 48]. [score:1]
Similarly, for NT3, our analysis identified significant increases in miR-21-5p and miR-221-3P in VO rat muscle. [score:1]
The miRNAs that exhibited a different response in VO rat muscle from what is seen with experimental denervation are miR-1, which in experimental denervation increases [48] but in VO rat muscle was observed to decline, and miR-221, which does not change with denervation [47] but was observed to increase in VO rat muscle. [score:1]
In VO rat muscle, miR-21-5p and miR-221-3p were increased significantly (Fig.   5b). [score:1]
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[+] score: 9
Cerda et al. found both atorvastatin and simvastatin down-regulate the expression of miR-221 [15]. [score:6]
Furthermore, miR-221 has been observed to impair proliferation of CD34 -positive haematopoietic progenitor cells by reducing expression of c-kit receptor factor [16]. [score:3]
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26
[+] score: 8
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-129-1, rno-mir-139, rno-mir-143, rno-mir-145, rno-mir-146a, rno-mir-206, 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
Conversely, knockdown of miR-221 and miR-22 in ERα -negative MDA-MB-468 partially restored ERα protein expression and increased tamoxifen -induced apoptosis [212]. [score:4]
Two miR-221 and miR-222 seed elements were identified in the 3’UTR of ERα and transfection of miR-221 and miR-222 suppressed ERα protein, but not mRNA in ERα positive MCF-7 and T47D cells. [score:3]
miR-221/222 was recently reported to be higher in ERα negative than ERα positive breast cancer cell lines and human breast tumors [212]. [score:1]
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27
[+] score: 8
Picking out 7 miRNAs associated with heart failure and taking statistical analysis, we found that Shenfu injection could significantly downregulate the levels of rno-miR-30c-1-3p, rno-miR-125b-5p, rno-miR-133a-5p, rno-miR-199a-5p, rno-miR-221-3p, rno-miR-146a-5p, and rno-miR-1-3p (Figure 5(b)). [score:4]
Picking out 7 miRNAs associated with heart failure and taking statistical analysis, our data reveal that Shenfu injection could significantly downregulate the levels of rno-miR-30c-1-3p, rno-miR-125b-5p, rno-miR-133a-5p, rno-miR-199a-5p, rno-miR-221-3p,rno-miR-146a-5p, and rno-miR-1-3p. [score:4]
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28
[+] score: 7
Similarly, the specific miRNA profile of AFL consisted of five downregulated (miR-93, miR-451, miR-221, miR-17-5p and miR-146a) and three upregulated (miR-200c, miR-490 and miR-195) miRNAs, in comparison to the control group. [score:7]
[1 to 20 of 1 sentences]
29
[+] score: 6
Other miRNAs from this paper: rno-mir-222, rno-mir-224
In the light of the above findings, and as demonstrated for other miRNAs, such as miR-221 and miR-222 [35- 37], miR-224 seems to have a dual mode of action that depends on the type of cancer involved: it acts as an onco-miR in some cancers and as an oncosuppressor-miR in others, suggesting that different molecular targets and networks are regulated by miR-224 in different neoplastic scenarios. [score:6]
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30
[+] score: 6
In contrast, other reports have shown that BIM is downregulated by miR-24 [50], and miR-221 [51], which inhibited apoptosis. [score:6]
[1 to 20 of 1 sentences]
31
[+] score: 6
Among these dysregulated miRNAs, miR-378 was downregulated while miR-221 expression increased in aHSCs compared to qHSCs, consistent with previous reports 18, 19 and demonstrating the reliability of our microarray data. [score:6]
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32
[+] score: 6
Stroke patients and atherosclerosis subjects showed significantly lower miR-221 serum levels than healthy controls[80] Rno-miR-873 Late (7d) miR-873 was up-regulated after onset of focal cerebral ischemia in mice[63] Rno-miR-223 miR-223 targeted glutamate receptors in mice brain. [score:6]
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33
[+] score: 6
12 of these miRNAs were ≥50% up-regulated in both groups with particularly strong increases in expression for miR-199a, miR-21, miR-214, miR-221, miR-222, and miR-31 (Figure 2B). [score:6]
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34
[+] score: 5
Although different technological platforms have been used for miRNA profiling, there is significant overlap between prognostic signatures described in previous work and several miRNAs that were later identified by more than three independent studies as being downregulated in essential hypertension or associated with vascular remo deling (e. g., miR-221, miR-26a, miR-21, miR-296-5p, and miR-204) [21– 24]. [score:4]
Some miRNAs, including miR-1, miR-145, miR-122, miR-221, and miR-222, have been linked to vascular endothelial dysfunction [12]. [score:1]
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35
[+] score: 5
We then used a screening system based on the luciferase reporter plasmid carrying the full-length 3′UTR of the FSHb mRNA and found that 18 miRNAs, specifically miR-433-3p, miR-323-3p, miR-328a-3p, miR-3573-3p, miR-204-5p, miR-206-5p, miR-31a-5p, miR-7a-5p, miR-880-3p, miR-186-5p, miR-503-5p, miR-383-5p, miR-324-5p, miR-505-5p, miR-27b-3p, miR-221-5p, miR-320-3p and miR-21-3p, could suppress the expression of the reporter by more than 30% (Figure 1). [score:5]
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36
[+] score: 5
Also, based on our recent finding that epithelial NGF expression is controlled via epigenetic mechanisms [38], we are testing the hypothesis that prenatal RSV infection interferes with the NGF promoter via suppression of specific miRNAs (especially miR-221) and selective demethylation, and that these effects are maintained by the postnatal persistence of virus in the developing lungs. [score:5]
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37
[+] score: 5
Notably, cardiac-specific miR-1, miR-133, miR-208 and miR-499 were all suppressed by two or more orders of magnitude [34], [35], as were the stemness and cell cycle repressors miR-141 and miR-137 [36]; in contrast, the proliferative miRNAs, miR-222 [37], increased dramatically in MDCs, and miR-221 was undetectable in myocytes but highly expressed in MDCs (Figure 5D). [score:5]
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38
[+] score: 5
Overexpression of miR-125b [16] would inhibit osteogenic differentiation while anti-miR-221 [17] intervention would trigger the osteogenic differentiation. [score:5]
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39
[+] score: 4
Recently, Li et al. reported that 16 miRNAs including miR-34, miR-199a-5p, miR-221, miR-146b, and miR-214 showed progressive up-regulation in rat with hepatic fibrosis caused by dimethylnitrosamine [30]. [score:4]
[1 to 20 of 1 sentences]
40
[+] score: 4
Under hyperglycemic conditions, miR-221 is induced in the HUVECs, which triggers the inhibition of the c-kit and impairs the HUVEC migration. [score:3]
Increasing evidence, predominantly from animal mo dels of diabetes, shows that several fibrosis-related miRNAs, including miR-192 [10, 11], miR-21 [12], miR-377 [13], and miR-221 [14], are involved in hyperglycemic conditions in different intrinsic renal cell types. [score:1]
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41
[+] score: 4
Recent studies have identified that many miRs [11], such as miR-1, miR-21, miR-29, miR-31, miR-143/145, and miR-221/222, play important roles in neointimal hyperplasia by regulating the functions of VSMCs. [score:2]
A number of miRs, such as, miR-1, miR-21, miR-29, miR-31, miR-143/145 and miR-221/222, were verified to be involved in neointimal hyperplasia by regulating the functions of VSMCs [11]. [score:2]
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42
[+] score: 3
Other miRNAs from this paper: rno-mir-222
miR-221 and miR-222 promote Schwann cell proliferation and migration by targeting LASS2 after sciatic nerve injury. [score:3]
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43
[+] score: 3
MiR-221 and miR-130a regulate lung airway and vascular development. [score:3]
[1 to 20 of 1 sentences]
44
[+] score: 3
miR-221 and miR-222 promote Schwann cell proliferation and migration by targeting LASS2 after sciatic nerve injury. [score:3]
[1 to 20 of 1 sentences]
45
[+] score: 3
For example, it has been reported that miR-221 [15], miR-199a/b [16][17], miR-27b [18], miR-195 [11] and miR-34a/b/c [19] positively regulate cardiac hypertrophy, while miR-378 [9], miR-29 [20], miR-150 [11], miR-223 [21] and miR-1 [22] negatively regulate cardiac hypertrophy. [score:3]
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46
[+] 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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47
[+] score: 3
Yu B miR-221 and miR-222 promote Schwann cell proliferation and migration by targeting LASS2 after sciatic nerve injuryJ. [score:3]
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48
[+] score: 3
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]
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49
[+] score: 3
For example, miR-195, miR-497, and miR-30b were found to be enriched in the cerebellum whereas miR-218, miR-221, miR-222, miR-26a, miR-128a/b, miR-138 and let-7c were highly expressed in the HIP. [score:3]
[1 to 20 of 1 sentences]
50
[+] score: 3
Fornari F In hepatocellular carcinoma miR-221 modulates Sorafenib resistance through inhibition of caspase-3 mediated apoptosisClin Cancer Res. [score:3]
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51
[+] score: 3
Emerging data support that micro -RNA, including miR-22 [23], miR-34a [24], miR-155 [25], miR-221/222 [26], is important for the multiple functions of statins, which is independent of HMG-CoA reductase inhibition. [score:3]
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52
[+] score: 3
miR-21, miR-155 and miR-221/222 have recently been shown to regulate AngII signaling in cardiac fibroblasts [14– 16] and in endothelial cells [17], while miR-29 regulates fibrotic pathways [18]. [score:3]
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53
[+] score: 2
Serum microrna-21 and microrna-221 as potential biomarkers for cerebrovascular disease. [score:2]
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54
[+] score: 2
Other miRNAs from this paper: rno-let-7f-1, rno-let-7f-2, rno-mir-141, rno-mir-146a, rno-mir-146b
Zhou YL Liu C Dai XX Zhang XH Wang OC Overexpression of miR-221 is associated with aggressive clinicopathologic characteristics and the BRAF mutation in papillary thyroid carcinomasMed Oncol. [score:2]
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55
[+] score: 2
Other miRNAs from this paper: mmu-mir-221, mmu-mir-222, rno-mir-222
MIR221/MIR222 -driven post-transcriptional regulation of P27KIP1 and P57KIP2 is crucial for high-glucose- and AGE -mediated vascular cell damage. [score:2]
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56
[+] score: 2
Of those, 9 miRNAs (let-7c-1, miR-221-3p, miR-221-5p, miR-222-3p, mir-322-2, mir-34c, miR-384-5p, mir-496, and mir-542-1) reported consistent directional changes as our data (15, 31– 33). [score:2]
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57
[+] score: 1
miR-145, miR-221, and miR-222 were selected based on their relationship with miR-143 and miR-223, respectively. [score:1]
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58
[+] score: 1
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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59
[+] score: 1
These data were consistent with the results obtained using a miR-221 sponge -based therapy in rat vein grafts [17]. [score:1]
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60
[+] score: 1
Other miRNAs from this paper: hsa-mir-221, mmu-mir-221
Lolli A Narcisi R Lambertini E Penolazzi L Angelozzi M Kops N Gasparini S van Osch GJ Piva R Silencing of antichondrogenic microRNA-221 in human mesenchymal stem cells promotes cartilage repair in vivoStem Cells. [score:1]
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61
[+] score: 1
The key miRNAs in rat LR confirmed in other papers such as miR-221 and miR-34a had the priority to be picked out, then circRNAs harbouring more than one above-mentioned miRNA binding sites were sorted out. [score:1]
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62
[+] score: 1
On the other hand, both EEP and Pn significantly inhibited in a dose -dependent manner the activation of HIF1 α. Finally, VEGF mRNA and microRNAs associated with angiogenesis in previous studies (miR-126, miR-19b, miR-221, miR-222, miR-27b, and miR-17) were evaluated by real-time PCR. [score:1]
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