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25 publications mentioning rno-mir-25

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-25. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 159
Other miRNAs from this paper: rno-mir-21, rno-mir-204, rno-mir-155
We found that LPS could down-regulate miR-25 expression, up-regulate PTEN and activate its downstream signaling pathway (TLR-4/NF-κB pathway), while overexpression of miR-25 reversed the effects, which illustrated that miR-25 could inhibit PTEN expression and TLR-4/NF-κB pathway induced by LPS. [score:15]
As shown in Figure 3A,B, LPS could down-regulate miR-25 expression and up-regulate the levels of PTEN, TLR4, and p-p65. [score:9]
Moreover, we found that overexpression of miR-25 could reverse the promoting effect of LPS on cardiomyocyte apoptosis, while overexpression of PTEN countered the inhibitory effect of miR-25 mimic on cardiomyocyte apoptosis. [score:7]
Moreover, LPS up-regulated the protein level of cleaved-caspase-3, and miR-25 mimic down-regulated its protein level. [score:7]
Contrarily, miR-25 mimic suppressed the luciferase reporter activity of PTEN 3′-UTR-WT and down-regulated the mRNA and protein levels of PTEN (Figure 5C). [score:6]
Previous studies have also found that miR-25 expression is down-regulated in patients with sepsis [8, 9]. [score:6]
These results indicated that LPS might promote inflammation by repressing miR-25 expression, increasing PTEN expression and activating the TLR-4/NF-κB signaling pathway. [score:5]
We found that LPS reduced the expression of miR-25, and overexpression of miR-25 reversed this effect (Figure 4A). [score:5]
As shown in Figure 4C, LPS promoted the expressions of TNF-α and IL-6, and overexpression of miR-25 reversed this effect. [score:5]
Moreover, luciferase reporter assay demonstrated that miR-25 inhibitor significantly increased the luciferase reporter activity of PTEN 3′-UTR-WT and up-regulated the mRNA and protein levels of PTEN (Figure 5B). [score:5]
Our study provided new evidences that miR-25 inhibited LPS -induced cardiomyocyte apoptosis by regulating PTEN and its downstream signaling pathway. [score:4]
In conclusion, miR-25 might inhibit the activation of inflammatory cells by regulating PTEN/TLR4/NF-κB axis, thereby reducing the apoptosis of cardiomyocytes and relieving LPS -induced myocardial injury. [score:4]
These findings proved that miR-25 could directly target PTEN. [score:4]
These results indicated that miR-25 might regulate the sepsis process by inhibiting inflammation. [score:4]
These results indicated that miR-25 could inhibit LPS -induced cardiomyocyte apoptosis by regulating PTEN. [score:4]
In the present study, we determined the expression of miR-25 and PTEN in different treated groups and detected how miR-25 regulated PTEN, and their effects on cardiomyocyte apoptosis. [score:4]
Moreover, miR-25 remarkably increased the survival rate of septic rats and inhibited inflammation. [score:3]
Liu et al. [7] found that miR-25 could inhibit cardiomyocyte apoptosis. [score:3]
Meanwhile, the expressions of TNF-α and IL-6 in miR-25 mimic group were lower than that in pre-NC group at each time point (Figure 2B,C). [score:3]
Additionally, we detected that miR-25 expression in serum of septic rats was significantly decreased, which was consistent with previous reports [8, 9]. [score:3]
The expression of miR-25 was decreased in serum of septic rats. [score:3]
MiR-25 directly targetted PTEN. [score:3]
In this study, PTEN was confirmed as the target gene of miR-25 for the first time. [score:3]
To verify whether miR-25 directly targetted PTEN, luciferase reporter assay was performed. [score:3]
The current study demonstrated that the levels of TNF- and IL-6 in the serum of septic rats and in LPS -induced cardiomyocytes were increased, while the levels were decreased significantly after transfecting miR-25 mimic, which indicated that miR-25 could alleviate myocardial injury caused by sepsis through inhibiting inflammatory reaction. [score:3]
H9C2 cells were treated with LPS for 24 h. MiR-25 mimic, miR-25 inhibitor, and pcDNA-PTEN were synthesized by GenePharma (Shanghai, China). [score:3]
MiR-25 has been found as an inhibitor for cardiomyocyte apoptosis induced by hypoxia/re-oxygenation [7], which suggest that miR-25 may be related to myocardial function. [score:3]
Moreover, LPS increased the levels of PTEN, TLR4, and p-p65, and overexpression of miR-25 reversed this effect (Figure 4B). [score:3]
MiR-25 inhibited H9C2 cells’ apoptosis induced by LPS. [score:2]
As shown in Figure 1A, miR-25 expression in CLP group was reduced significantly compared with sham group. [score:2]
MiR-25 expression was reduced in H9C2 cells induced by LPS. [score:2]
These suggested that miR-25 might be an important regulator in myocardial function. [score:2]
Then, miR-25 mimic or miR-25 inhibitor and reporter plasmids were co -transfected into cells using Lipofectamine 2000 (Invitrogen) for 48 h. The luciferase activities were determined using a luciferase reporter assay system (Promega) according to the manufacturer’s instructions. [score:2]
Figure 2Septic rats were divided into pre-NC group and miR-25 mimic group (n=21). [score:1]
org), miR-25 could bind to 3′-UTR of PTEN (Figure 5A). [score:1]
U6 snRNA served as an internal normalized reference for miR-25, and β-actin used as an internal control for PTEN and TLR4. [score:1]
H9C2 cells were separately divided into four groups, namely control, LPS, pre-NC, and miR-25 mimic groups. [score:1]
Figure 4H9C2 cells were separately divided into four groups, namely control, LPS, pre-NC, and miR-25 mimic groups. [score:1]
MiR-25 regulated the survival rate and inflammation in rats. [score:1]
However, whether miR-25 is involved in the pathogenesis of SIMD remains unknown. [score:1]
To investigate the effect of LPS on the expressions of miR-25, PTEN, and TLR4, H9C2 cells were treated with LPS for 24 h. The control group was not given any treatment. [score:1]
Pan et al. [18] reported that miR-25 could protect cardiomyocytes from oxidative damage. [score:1]
As shown in Figure 6A, LPS promoted H9C2 cardiomyocytes’ apoptosis, and miR-25 mimic could counter this effect. [score:1]
showed that the survival rate in miR-25 mimic group was significantly higher than that in pre-NC group (Figure 2A). [score:1]
MiR-25 regulated TLR-4/NF-κB pathway and inflammation. [score:1]
Figure 6(A) LPS promoted H9C2 cardiomyocytes apoptosis, and miR-25 mimic could counter this effect. [score:1]
Thus, we speculated that miR-25 might be a meaningful biomarker for sepsis. [score:1]
The others were separately divided into pre-NC group and miR-25 mimic group (n=21), and both groups of rats were divided into three subgroups (n=7) at different time points after the operation (24, 48, and 72 h). [score:1]
However, the mechanisms of miR-25 in sepsis have not been thoroughly revealed. [score:1]
Rats in miR-25 mimic group were treated with miR-25 mimic (10 μl) by tail intravenous injection. [score:1]
Septic rats were divided into pre-NC group and miR-25 mimic group (n=21). [score:1]
Therefore, our study enriches the literature that supports miR-25 playing an important role in sepsis. [score:1]
[1 to 20 of 52 sentences]
2
[+] score: 128
Other miRNAs from this paper: rno-mir-93, rno-mir-106b
Therefore, we hypothesized that rTMS would increase the expression of miR-25 and repress the expression of its targets, thereby promoting adult NSC proliferation and inhibiting cell-cycle arrest after focal cerebral ischemia. [score:9]
The results revealed that (1) miR-25 levels in the mo del group were up-regulated 2.3-fold relative to the levels in the sham-operated group (2.55 versus 1.09, p<0.001), and (2) the miR-25 expression level in the rTMS group was also significantly up-regulated 4.3-fold relative to the sham-operated group (4.65 versus 1.09, p<0.001) and 1.8-fold relative to the mo del group (4.65 versus 2.55, p<0.001). [score:9]
After Ant-25 was introduced, the results revealed that the protein level of p57 was remarkably up-regulated in the ipsilateral cortex, confirming the direct suppression of p57 by miR-25. [score:7]
Additionally, adult NSC proliferation has been suppressed in ischemic SVZs after 10 Hz rTMS treatment due to miR-25 knockdown accompanied by elevated expression of p57. [score:6]
In this study, we found that 10 Hz rTMS could promote the proliferation of NSCs in the SVZ after focal cerebral ischemia, and miR-25 was significantly up-regulated after rTMS treatment, while the proliferation of NSCs in SVZ was blocked by the inhibition of miR-25. [score:6]
The effect of ICV injection of Ant-25 treatment on the upregulation of miR-25 target gene p57 was demonstrated by Western blotting analysis. [score:6]
Effects of rTMS on miR-25 regulation of the expression of target genes p57 and PTEN. [score:6]
As previously mentioned, p57, co-operatively suppressed by miR-25, is a Cdk inhibitor (CKI) and mediates the transitions between cell-cycle phases by binding to Cdks. [score:5]
These data suggested that tMCAO slightly induced the up-regulation of miR-25 and that 10 Hz rTMS prominently strengthened this effect (Figure 5). [score:4]
Brett J O et al. carried out an elaborate study of the role of miR-106b∼25 in adult NSCs and noted that miR-25 knockdown decreases NSC proliferation and that miR-25 overexpression increases adult NSC proliferation [9]. [score:4]
This result suggested that 10 Hz rTMS played a regulatory role in the expression of miR-25. [score:4]
The consequent changes of p57 and PTEN, which can generate adult NSC proliferation, were observed in the mo del group, the sham-operated group, and the rTMS group (n = 5 for each group) to further verify the effects of rTMS on the miR-25 cluster and to demonstrate a direct interaction between the target genes and the candidate miRNAs. [score:4]
Although the miR-25/p57 pathway was demonstrated to play a role in the therapeutic mechanisms of rTMS for focal cerebral ischemia in the present study, there may even be crosstalk between the different pathways that are focused on miR-25 or targeted by the other two members of the miR-106b∼25 cluster. [score:3]
Expression changes of miR-25 in the ipsilateral cortex 7 days after surgery. [score:3]
The results showed that the levels of miR-25 were maintained at lower levels for 7 days after the injection of Ant-25, although miR-25 was not totally inhibited. [score:3]
rTMS altered the expression of miR-25 in the ischemic cortex. [score:3]
Our data revealed that depletion of miR-25 had some relevance to ICV injection concentrations of Ant-25 and that excessive or inadequate doses of antagomirs had differential impacts on miRNA expression. [score:3]
Additionally, Brett et al. 's group reported that the miR-106b∼25 cluster could promote the proliferation of adult NSCs mainly due to miR-25 [9], [10], which also appeared to be one of the strongly expressed miRNAs in the post-ischemic brain [11]. [score:3]
To examine possible changes of miR-25 in response to the rTMS treatment after tMCAO, levels of its expression were determined by qRT-PCR in the ipsilateral cortex for the mo del group, the sham-operated group, and the rTMS group (n = 5 for each group). [score:3]
To further demonstrate this hypothesis, we preliminarily tested the impact of miR-25 inhibition on its target proteins, investigated the effect of its deletion on the proliferation of adult NSCs with rTMS treatment after focal cerebral ischemia, and sequentially explored associated functions of miR-25 in vivo. [score:3]
Thus, our results clearly illustrated that the suppression of miR-25 blocked adult NSC proliferation after tMCAO (Figure 9). [score:3]
Thus, it is possible that miR-25 regulates adult NSCs by coordinately modulating networks, and further study is required to explore the full set of regulatory mechanisms of rTMS for cerebral ischemia. [score:3]
Hence, based on our results and theoretical support, we can assert that 10 Hz rTMS appears to facilitate the proliferation of adult NSCs after cerebral ischemia by promoting the expression of miR-25. [score:3]
p57 and PTEN were identified as miR-25 target genes [13], [14]. [score:3]
Here, we observed that the expression level of miR-25 in the ipsilateral cortex was significantly higher after 10 Hz rTMS than for the mo del group without rTMS. [score:3]
Combined with the other results, we provide novel evidence that miR-25 -dependent regulation of p57 influences the proliferation of adult NSCs induced by rTMS after focal cerebral ischemia. [score:2]
Depletion of miR-25 using antagomirs in vivo. [score:1]
Deletion of miR-25 blocked the proliferation of adult NSCs in the SVZ induced by rTMS. [score:1]
To determine whether miR-25 plays a pivotal role in rTMS's promotion of adult NSC proliferation after focal cerebral ischemia, ICV injections of Ant-25 and Scr were used at different doses just prior to tMCAO, followed by 7 days of rTMS treatment. [score:1]
The protective effect of rTMS was associated with the miR-25/p57-signaling pathway. [score:1]
In this paper, we reported that miR-25 is a crucial participant in promoting the effects of rTMS on adult NSC proliferation after focal cerebral ischemia in rats. [score:1]
MiR-25 belongs to the miR-106b∼25 cluster. [score:1]
0109267.g007 Figure 7(A– C) A) miR-93, B) miR-106b and C) miR-25 levels in the ischemic cortex after ICV injection of 1 nmol, 2.5 nmol and 4 nmol of Ant-25 or Scr. [score:1]
Recently, our group found that miR-25 increased significantly after 10 Hz rTMS treatment of cerebral ischemia in rats. [score:1]
In fact, miR-106b and miR-93 have the same seed sequence and similar 3′-halves, whereas miR-25-lacking the same sequence-is expected to have a separate function [12]. [score:1]
Taken together, the activation of miR-25 could promote a proliferation state of adult NSCs through p57, and these findings lead us to conclude that rTMS mainly induces the activation of the miR-25/p57 pathway, thereby promoting adult NSC proliferation after focal cerebral ischemia. [score:1]
In addition, the current study also reveals an interesting effect of different doses of antagomir-25 and its scrambled antagomir on the miRNA levels of miR-25 and the unrelated miR-93 and miR-106b. [score:1]
Depletion of miR-25 using antagomirs in vivo To determine whether miR-25 plays a pivotal role in rTMS's promotion of adult NSC proliferation after focal cerebral ischemia, ICV injections of Ant-25 and Scr were used at different doses just prior to tMCAO, followed by 7 days of rTMS treatment. [score:1]
A dose of 2.5 nmol Ant-25 significantly reduced miR-25, whereas 1 nmol had no effect (Figure 7A, D), and neither dose of Scr had an effect on miR-25 levels (Figure 7A, D). [score:1]
This cluster is located within an intronic region of the Mcm7 gene and codes for three different mature miRNA species: miR-106b, miR-93 and miR-25. [score:1]
These factors suggest that miR-25 may be an important agent in rTMS for promoting adult NSC proliferation after focal cerebral ischemia. [score:1]
All data suggest that miR-25 plays an important role in the therapeutic effects of rTMS on NSC proliferation in the SVZ after focal cerebral ischemia and that rTMS has potential in the rehabilitation of neural function after focal cerebral ischemia. [score:1]
0109267.g005 Figure 5(A) Electrophoresis of miR-25 and U6 on gel. [score:1]
[1 to 20 of 43 sentences]
3
[+] score: 54
The results showed that 14 miRNAs (miR-30a-5p, miR-30e-5p, miR-425-5p, miR-142-3p, miR-191a-3p, miR-215, miR-29b-3p, miR-30b-5p, miR-26a-5p, miR-345-5p, miR-361-5p, miR-185-5p, miR-103-3p) were down-regulated but no miRNA was up-regulated among above three altered miRNAs from microarray in OVX serum by normalizing to miR-25-3p (Fig. 3b). [score:7]
In present, we verified miR-25-3p as a stable reference endogenous control gene and 4 downregulated biomarkers from women with normal BMD, osteopenia and osteoporosis. [score:4]
In addition, miR-328-3p also showed a notable decrease in osteoporotic patients in our study by normalizing to miR-25-3p (Fig. 4a), which was reported down-regulation in the serum of postmenopausal osteoporotic fracture and involved in bone formation by Weilner et al. 13. [score:4]
The expression of miR-25-3p was also detected in the head down bedrest monkeys with osteoporosis due to mechanical unloading and showed no significant difference from that in the control groups (Fig. 2e). [score:3]
Therefore, the consensus of the unchanging expression signature of miR-25-3p in serum proved that miR-25-3p should be a suitable reference gene of serum miRNAs for osteoporosis. [score:3]
Moreover, our results conformed the finding of Seeliger et al. 12 who reported no differential expression of miR-25-3p in serum between non-osteoporotic and osteoporotic fracture patients. [score:3]
Similarly, no significant change of serum miR-25-3p expression was found among postmenopausal women with normal BMD, osteopenia or osteoporosis (Table 1 and Fig. 2f). [score:3]
showed that there were no significant differences of miR-25-3p expression in those paired subjects. [score:3]
Serum was collected from different stage at 1 [st] to 6 [th] week and the expression levels of 4 top ranked miRNAs (miR-25-3p, miR-140-5p, miR-342-5p and miR-150-5p) were assayed by qPCR. [score:2]
The qPCR results of miR-25-3p expression showed no marked change compared with their control (Fig. 2i,j). [score:2]
Identified miR-25-3p as the suitable reference gene for osteoporosis. [score:1]
Therefore, ten miRNAs (miR-19b-3p, miR-21-5p, miR-25-3p, miR-30a-5p, miR-133b-3p, miR-140-5p, miR-150-5p, miR-199a-3p, miR-342-5p, miR-3473) were chosen as candidate reference genes. [score:1]
In addition, the expression pattern of miR-25-3p during osteoclast and osteoblast differentiation was investigated in vitro. [score:1]
miR-25-3p was also detected in rhesus monkeys after long-duration bedrest and postmenopausal women with osteoporosis. [score:1]
miR-25-3p was identified as the most suitable reference gene and expanded its application scope to both estrogen deficiency- and mechanical unloading- induced osteoporosis. [score:1]
Ssa-miR-25-3p was identified as the most suitable single reference gene in Atlantic salmon 29. [score:1]
Given this, miR-25-3p was detected in the femur of HU and OVX rats (Fig. 2gh). [score:1]
Recently, Das et al. reported miR-25-3p was the most suitable reference gene in human cancer cell lines and even more stable than RNU6 28. [score:1]
miR-25-3p was recommended as the most suitable reference gene according to the ranking of 9 candidate miRNAs by two statistical algorithms (geNorm and NormFinder). [score:1]
Obviously, miR-25-3p was rather stable in both algorithms, and was recommended as reference gene by comprehensive ranking. [score:1]
Conversely, miR-140-5p, miR-342-5p and miR-150-5p were not as stable as miR-25-3p and showed some notable changes at some stage (Fig. 2c). [score:1]
During HU within 6 weeks, miR-25-3p was the most stable gene and showed no significant difference between any pair matched groups (p > 0.05). [score:1]
With this algorithm, miR-140-5p was identified as the most stable gene, followed by miR-25-3p (Fig. 2b). [score:1]
The stability of miR-25-3p was further validated at different stage of HU osteoporotic mo dels in another independent experiment. [score:1]
To extend its application scope, we further estimated the stability of miR-25-3p in various osteoporosis mo dels and species. [score:1]
Indeed, miR-25-3p showed no marked alterations in the femur of OVX or HU rats, as well as during osteogenic or osteoclastic differentiation. [score:1]
By geNorm, miR-25-3p was ranked as the most stable gene and a combination of miR-25-3p, miR-342-5p and miR-140-5p was recommended for optimal normalization (Fig. 2a). [score:1]
To examine whether miR-25-3p is also stable in some extended osteoporotic mo dels, including OVX rats, monkey after head down bedrest and postmenopausal women, serum was collected from each osteoporotic mo del. [score:1]
All these results confirmed miR-25-3p was a suitable reference gene of serum miRNAs for osteoporosis. [score:1]
Validation of miR-25-3p as suitable reference gene in osteoporotic mo dels. [score:1]
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4
[+] score: 48
The expression levels of RB1 and PTEN were downregulated following miR-106b and miR-93 transfection in both BRL and RH-35 cells, while the levels of CEBPA and KAT2B were downregulated after miR-25 transfection. [score:9]
As we expected, miR-106b, miR-93, miR-25 and miR-92a were significantly up-regulated at 24 and 36 hours after 2/3 PH, and miR-101a was down-regulated at 12, 24 and 36 hours after 2/3 PH (Supplementary Figure 5). [score:7]
In details, miR-101a was down-regulated, and it decreased cell number in the G2-M phase with consistently increases in cell number in the G1 or S phases; meanwhile, miR-92a, miR-25, miR-93, and miR-106b were up-regulated, and they decreased the G1 cell population while concomitantly increasing the accumulation of cells in the S and G2 phases. [score:7]
As shown in Fig. 8C, miR-106b and miR-93 expression significantly reduced the luciferase activities of RB1 reporters by 48% and 44%, respectively, and miR-25 reduced luciferase expression of KAT2B reporters by 41%. [score:5]
BRL cells transfected with a vector harboring the AAV9-miR-106b~25 cluster expressed more miR-25, miR-93, and miR-106b than cells transfected with the AAV9 cluster control vector, as assessed using real-time PCR (Fig. 6B). [score:3]
Taken together, these results show that RB1 and KAT2B are targets of miR-106b/93 and miR-25, respectively. [score:3]
We identified RB1 and KAT2B as novel targets of miR-106b/93 and miR-25, respectively. [score:3]
The miR-106b~25 cluster vector (pAOV-mCherry-cluster, Fig. 6D) expressed mCherry, miR-25, miR-93 and miR-106b. [score:3]
Thus, these significantly altered miRNAs were analyzed for their role in the cell cycle; these analyses showed that miR-25, miR-93, and miR~106b were associated with faster entry into the S and G2 phases. [score:1]
Interestingly, miR-25, miR-93, and miR-106b are members of the miR-106b~25 cluster located within about 0.5 kb on chromosome 12 (Fig. 6A). [score:1]
As demonstrated above, miR-92a, miR-25, miR-93, and miR-106b are associated with faster entry into the S and/or G2 phases. [score:1]
We found that miR-106b, miR-93, and miR-25 levels remained higher after PH in the livers of rats injected with miR-cluster than in the livers of control rats; and miR-106b, miR-93 and miR-25 were significantly lower in the miR-sponge -treated rats than that in the controls, especially at 24h and 36 h after 2/3PH (Supplementary Figure 6). [score:1]
A total number of 11 and 16 miRNA–mRNA pairs were identified for miR-25 and miR-93 (miR-106b), respectively. [score:1]
However, CEBPA reporter luciferase activities were not repressed by miR-25. [score:1]
In control rats, we found that miR-106b, miR-93, and miR-25 levels also increased after 2/3 PH (Supplementary Figure 6). [score:1]
AAV9-miR-106b~25 sponges are transcripts with 6 repeated miRNA antisense sequences of miR-25, miR-93 and miR-106b (Fig. 6C). [score:1]
[1 to 20 of 16 sentences]
5
[+] score: 39
0180490.g006 Fig 6 UNX combined with HSD intake upregulates AT1R, LTCCs leading to increased cardiovascular reactivity and decreased BRS; upregulates miR-25, miR-155 and miR-451 and downregulates miR-99b affecting SERCA2, AKT and AMPK leading to impaired excitation-coupling cycle, fibrosis and hypertrophy culminating in cardiac dysfunction. [score:10]
UNX combined with HSD intake upregulates AT1R, LTCCs leading to increased cardiovascular reactivity and decreased BRS; upregulates miR-25, miR-155 and miR-451 and downregulates miR-99b affecting SERCA2, AKT and AMPK leading to impaired excitation-coupling cycle, fibrosis and hypertrophy culminating in cardiac dysfunction. [score:10]
Hence, we checked the expression of miR-25, which targets SERCA2 in the heart and interestingly, we observed its level increased in HSD and UNX+HSD demonstrating the involvement of miR-25 in escalating LVEDP in these groups. [score:5]
This cardiac dysfunction is attributed to the activation of local RAS, altered cardiac miRNA-25, -99b, -155, -451 and their corresponding targeted proteins—SERCA2, p-AKT, and p-AMPK (Fig 6). [score:3]
miR-25, which targets SERCA2 [14], was found to be increased in the animals fed with high salt diet. [score:3]
High salt feeding alters micro RNA levels (miR-25, -155, -99b, -451) which regulate SERCA, AKT and AMPK. [score:2]
However, we failed to observe any positive correlation between the tissue and circulating levels of miR-25, -99b and -451 in our study. [score:1]
D), E) Relative levels of miR-25, miR-155, miR-451 and miR-99b in heart normalized with sn-RNU5G; F) Relative levels of miR-25, miR-451 and miR-99b in plasma normalized with miR-30e. [score:1]
Micro RNAs quantified were hsa-miR-25-3p (Cat# 204361), mmu-miR-155-5p (Cat# 205930), hsa-miR-99b-3p (Cat# 204064) and mmu-miR-451(Cat# 204734) and normalized with RNU5G (a small nuclear RNA) in heart and hsa-miR-30e-5p (Cat# 204714) in plasma. [score:1]
Declined cardiac function in heart failure is attributed to decreased SERCA2, which in turn is due to increased endogenous miR-25 in mice and humans [14]. [score:1]
To check whether the pattern of miRs obtained in heart is correlating with that of plasma or not, we assessed the levels of miR-25, -99b, -155, and 451 in plasma. [score:1]
Roles of miR-25 [14], miR-155 [15] & miR-451 [16] in various murine CVDs have been reported but their role in high salt diet -induced CV complications in uninephrectomized rats is not yet reported. [score:1]
[1 to 20 of 12 sentences]
6
[+] score: 14
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]
[1 to 20 of 2 sentences]
7
[+] score: 13
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-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-221, 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]
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]
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]
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8
[+] score: 11
Recently, Gurha [30] showed that genetic ablation of miRNA-22 indirectly modulates Serca-2a expression, and Wahlquist [31] showed that miRNA-25 also indirectly regulates Serca-2a expression and contributes to impaired cardiac function during heart failure. [score:8]
Wahlquist C, Jeong D, Rojas-Muñoz A, Kho C, Lee A, Mitsuyama S, et al. Inhibition of miR-25 improves cardiac contractility in the failing heart. [score:3]
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9
[+] score: 10
For example, miR-106b, miR-21, miR- 22, miR-19b and miR-25 are known to regulate PTEN and miR-27 and miR-139 repress FoxO1 translation through direct binding to the 3′-UTR [31], [32], [33], [34], [35], [36], [37], [38]. [score:5]
Among the up-regulated miRNAs, miR-106b, miR-25 and miR-19b share the same primary transcripts, and miR-24 and miR-27 share primary transcripts. [score:4]
We have also noticed that miRNAs previously detected in neurites such as miR-134, miR-25 and miR-26a showed changes at 24 h after contextual conditioning [17], [19]. [score:1]
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10
[+] score: 9
We found that expression of many miRNAs (miR-24, miR-25, miR-7a, miR-103, miR-17-5p, miR-106b, miR-93, miR-206 and miR-133b) changed significantly during conditions of UPR in cardiomyoblasts. [score:3]
We observed that changes in the expression of nine miRNAs (miR-24, miR-25, miR-7a, miR-103, miR-17-5p, miR-106b, miR-93, miR-206 and miR-133b) analyzed by qRT-PCR were consistent with those by miRNA microarray at p < 0.05 (Figure 3). [score:3]
In agreement with our previous results we observed reduced expression of all three miRNAs (mir-106b, miR25 and miR-93) belonging to the miR-106b-25 cluster during conditions of UPR in H9c2 cells. [score:3]
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11
[+] score: 7
Recently, Gurha et al. (2012) [45], showed that genetic ablation of miRNA-22 regulates target proteins that function as transcription factors for SERCA2a expression, and Wahlquist et al. (2014) [46], showed that miRNA-25 regulates SERCA2a and contributes to declining cardiac function during heart failure. [score:7]
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[+] score: 7
Furthermore, 40 of the miRNAs, including miR-34b-3p, miR-25-3p, miR-126-5p, miR-142-5p, and miR-324-5p, were only transiently upregulated (Figure  2A); the other 23 miRNAs, including miR-34a-3p and miR-324-5p, were transiently downregulated on the 3rd day but returned to normal levels by the 14th day (Figure  2B). [score:7]
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13
[+] score: 6
Regulation of NADPH oxidase activity is associated with miRNA-25 -mediated NOX4 expression in experimental diabetic nephropathy. [score:4]
In a similar context, the observation that microRNA miR-25 may contribute to the negative regulation of Nox4 has been reported in diabetic nephropathy (Fu et al., 2010). [score:2]
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14
[+] score: 5
MicroRNA expression in human airway smooth muscle cells: role of miR-25 in regulation of airway smooth muscle phenotype. [score:4]
We found miR-25 decreased after exercise, which could be related to the inflammatory state caused by acute aerobic exercise. [score:1]
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15
[+] score: 4
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-15a, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-27b, rno-mir-29a, 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-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
The prospect that a similar function may extend to other miRNAs is suggested by the conservation of several miRNAs (e. g. miR-25, miR-34a/b/c, miR-135a/b, miR-194, and miR-200a) that are capable of directly targeting the Wnt/β-catenin, a signaling pathway that has been wi dely implicated in the control of oncogenic hallmarks such as cell proliferation, metastasis, angiogenesis, telomerase activity, and apoptosis (reviewed by [49]). [score:4]
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[+] score: 3
The pattern of coordinated reduction in expression of miR-25, miR-93, and miR-106b (Table 1) is due to the clustering of these three miRNA genes at intron 12 of Mcm7 on chromosome 12. [score:3]
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[+] score: 3
Of the four miRNAs selected for Pik3cb, expression of two, miR-25-3p and miR-130a-3p, was reduced (p < 0.05 and p < 0.001, respectively) in in vitro differentiated adipocytes from LP offspring (Fig.   5). [score:3]
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[+] score: 2
According to our in silico analysis, Ppar γ is likely regulated by microRNAs like let-7 family members, miR-30 family members, miR-27b, miR-23ab, miR-93, miR-25, miR-128ab, miR-320, and miR-135. [score:2]
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[+] score: 2
analysis confirmed the direction and amplitude of all miRNA changes with the exception of let-7d, miR-25*, miR-187, miR-291a-5p, miR-292-5p, miR-365, miR-431, miR-487b, miR-615-5p, miR-743a, miR-20b-3p, miR-199a-3p which remained unaltered or showed no statistical significance. [score:2]
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[+] score: 2
Other miRNAs from this paper: rno-mir-148b, rno-mir-21, rno-mir-26a, rno-mir-133a, rno-mir-148a
In a set of wheezing + LRI patients (n = 20) and age- and gender-matched LRI control children (n = 20), miR-21, miR-25, miR-26a, miR-133a and miR-148 showed potential statistical differences between the patient and control groups (p < 0.10) (Fig.   1a). [score:1]
b RT-qPCR results of miR-21, miR-25, miR-26a, miR-133a and miR-148 in plasma from 35 indifferent control, 35 LRI control and 70 wheezing + LRI children. [score:1]
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Among the spleen-specific miRNAs identified, five of them belong to the mir17 miRNA cluster, which comprise miR-17, miR-18, miR-19a, miR-19b, miR-20, miR-25, miR-92, miR-93, miR-106a, and miR-106b [59]. [score:1]
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[+] score: 1
Other anti-apoptotic miRs have also been recently identified, including miR-21 [12], miR-25 [28], and miR-378 [17]. [score:1]
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[+] score: 1
Zhang J MicroRNA-25 Negatively Regulates Cerebral Ischemia/Reperfusion Injury-Induced Cell Apoptosis Through Fas/FasL PathwayJ Mol Neurosci. [score:1]
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[+] score: 1
This cluster has two paralogs, miR-106a~363 (miR-106a, miR-18b, miR-19b-2, miR-20b, miR-92a-2 and miR-363, located on the X chromosome) and miR-106b~25 (miR-106b, miR-93, and miR-25, located on human chromosome 7), which are located on different chromosomes but contain individual miRNAs that are highly similar to those encoded by the miR-17~92 cluster [36, 37]. [score:1]
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25
[+] score: 1
Repetitive transcranial magnetic stimulation promotes neural stem cell proliferation via the regulation of MiR-25 in a rat mo del of focal cerebral ischemia. [score:1]
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