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9 publications mentioning rno-mir-410

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-410. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

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[+] score: 248
miR-410 is up-regulated by high fat diet and suppresses Smad 7 translation. [score:8]
The kidney- or adipose-derived circulating miR-410-5p down-regulates the protein expression of its target Smad 7 in the heart, resulting in the activation of the TGFβ signaling. [score:8]
Although the expression of miR-410-3p is induced in the cardiac disease mo dels of mice 31, 32, the expression of pre-miR-410 is not significantly altered in the heart of rats after HFD feeding. [score:7]
These results suggest that miR-410-5p targets Smad 7 for translational inhibition. [score:7]
Although overexpression of miR-410-5p did not obviously influence the mRNA expression of Smad 7 (Fig.   S2), it markedly suppressed the protein levels of Smad 7 (Fig.   5d,e). [score:7]
In contrast, the expression of pre-miR-410 is markedly up-regulated in the kidney and adipose tissues of rats fed HFD. [score:6]
Of the six most up-regulated miRNAs, we identified miR-410-5p that could bind to the 3′UTR of Smad 7 by using a miRNA target prediction algorithm (RNA22) (Fig.   5a). [score:6]
Furthermore, the expression of pre-miR-410 was significantly up-regulated only in the kidney and adipose tissues, but not in other tissues, after HFD feeding. [score:6]
To test whether miR-410-5p regulated Smad 7 endogenously, we determined the effect of miR-410-5p overexpression on Smad 7 expression in cardiocyte cell line H9c2. [score:6]
Our data indicate that the expression of miR-410-5p is significantly up-regulated in the heart of rats fed HFD. [score:6]
Therefore, it is likely that the expression of miR-410-5p is up-regulated in the donor tissues, kidney and adipose in obese rats, and secreted into the bloodstream by packing into exosomes or binding to AGO2. [score:6]
Clark et al. have demonstrated that miR-410-3p is significantly upregulated in the cardiac disease mo dels of mice, including myocardial infarction and chronic angiotensin II stimulation, and in the cardiomyopathies associated with muscular dystrophies [31]. [score:6]
NPHS2-miR-410, kidney-specific overexpression; aP2-miR-410, adipocyte-specific overexpression. [score:5]
miR-410-5p probably derived from the kidney or adipose tissues negatively regulates the protein expression of Smad-7 in the heart through direct base pairing to the 3′ UTR of its mRNA (Fig.   8). [score:5]
Overexpression of miR-410-3p induces apoptosis by targeting high-mobility group box 1 protein in cardiac myocytes. [score:5]
As shown in Fig.   S4a, tissue-specific overexpression of miR-410-5p led to a significant increase in miR-410-5p expression in kidney or adipose tissue. [score:5]
Inhibition of Smad 7 protein expression by miR-410-5p leads to the activation of the TGFβ signaling, induction of fibrotic genes, and subsequent cardiac fibrosis. [score:5]
Next, we determined the mRNA levels of CTGF, Col1α1, Col3α1, and Col4α1 by qPCR and found significant up-regulation of all four gene transcripts in the heart of miR-410-5p -treated rats (Fig.   6d). [score:4]
Thus, miR-410-5p represents a promising candidate to regulate Smad 7. Figure 4The miRNA expression profiles in the heart of rats. [score:4]
We focused on miR-410-5p, which was markedly up-regulated in the cardiac tissues of rats fed HFD. [score:4]
Our in vitro and in vivo experiments demonstrate that miR-410-5p down-regulates the protein levels of Smad 7, resulting in activation the TGFβ signaling pathway and induction of fibrotic genes. [score:4]
miR-410-5p up-regulated in the kidney and adipose of obese rats is released into circulation. [score:4]
The up-regulation of miR-410-3p is also observed in a myocardial ischemia/reperfusion injury mice mo del and in hypoxia/reoxygenation -treated cultured human adult cardiac myocytes [32]. [score:4]
To elucidate the involvement of miR-410-5p in the regulation of Smad 7 expression, we construct a vector that contained wild-type of the Smad 7-3′-UTR of or a 5-bp mutation in the miR-410-5p seed sequence recognition site for luciferase reporter assays (Fig.   5a). [score:4]
More importantly, overexpression of miR-410-5p in either kidney or adipose increases the levels of miR-410-5p in the heart and exosomes. [score:3]
Rats fed normal diet were infected with 5 × 10 [8] TU of adenovirus particles containing empty vector or vector expressing pre-miR-410 through tail vein injection. [score:3]
Inhibition of miR-410-3p in stressed cardiomyocytes attenuates the hypertrophic response. [score:3]
We found that miR-410-5p activated the TGFβ signaling pathway by targeting Smad 7. Finally, our data showed that miR-410-5p from the kidney and adipose tissues probably induced cardiac fibrosis. [score:3]
The luciferase activity of Smad 7-3′-UTR was markedly inhibited in H9c2 cells after transfection of miR-410-5p (Fig.   5c). [score:3]
Finally, we tested the effect of kidney- or adipose-specific overexpression of miR-410-5p on cardiac fibrosis. [score:3]
Figure 5Smad 7 is a target gene of miR-410-5p. [score:3]
Lentivirus vectors expressing pre-miR-410 and miR-410-5p antimiR were obtained from GenePharma Co. [score:3]
Therefore, it is likely that miR-410-5p that expressed in the renal and adipose tissues is secreted into the bloodstream, and then transferred to the heart to induce cardiac fibrosis. [score:3]
Heart tissues from miR-410-5p overexpression group showed focal regions of fibrosis in the interstitium (Left panels). [score:3]
Twelve-week-old rats fed a standard laboratory chow were infected with 1 × 10 [8] TU of lentivirus particles containing empty vector PGLV3 or vector expressing pre-miR-410 through tail vein injection. [score:3]
Meanwhile, we found that overexpression of miR-410-5p in either kidney or adipose increased the levels of miR-410-5p in the heart and exosomes (Fig.   7e,f). [score:3]
Meanwhile, overexpression of miR-410-5p significantly promoted the phosphorylated levels of Smad 2 (Fig.   5d,e). [score:3]
To investigate the effect of elevated miR-410-5p expression on cardiac fibrosis, miR-410-5p was overexpressed in the whole body via lentiviral vector (PGLV3-miR-410). [score:3]
For adipocyte-specific overexpression, pre-miR-410 was inserted into the adenovirus vector pAV[Exp]-aP2 > EGFP containing the promoter of adipocyte-specific gene aP2/FABP4, resulting in the vector pAV[Exp]-aP2 > EGFP:{rmiR-410}. [score:3]
For kidney-specific overexpression, pre-miR-410 was inserted was inserted into the adenovirus vector pAAV[Exp]-NPHS2 > EGFP containing the promoter of kidney-specific gene NPHS2/Podocin, resulting in the vector pAV[Exp]- NPHS2 > EGFP:{rmiR-410}. [score:3]
Overexpression of miR-410-5p in both tissues induced cardiac fibrosis (Fig.   7g,h), which were accompanied with reduced protein levels of Smad 7 (Fig. S4b–d). [score:3]
When searching the tissue distribution of miR-410-5p in database [24], we found that miR-410-5p is only expressed in renal and adipose tissues. [score:3]
Adenovirus vectors for adipocyte- or kidney-specific overexpression of pre-miR-410 were obtained from Cyagen Co. [score:3]
It has been shown that miR-410-3p is highly expressed in the perinatal heart and sharply decreased in the adult heart, suggesting a role in perinatal cardiac function [30]. [score:3]
Two recent studies have link miR-410-3p to cardiac diseases 31, 32. [score:3]
As the expression of pre-miR-410 in the heart, liver, and muscle was much lower than those in the kidney and adipocyte, the elevated miR-410-5p levels in these tissues were probably derived from those in circulation released from renal and adipose tissues. [score:3]
Our results demonstrate that the expression of pre-miR-410 in the kidney and adipose tissues are much higher than that in the heart. [score:3]
Furthermore, overexpression of miR-410-5p in rats elicits cardiac fibrosis. [score:3]
As miR-410-3p functions as an oncogene or tumor suppressor gene in some malignancies [35], the degradation of miR-410-3p favors the tumor progression. [score:3]
In this study, miR-410-5p is identified by miRNA microarray analysis and the miRNA target prediction algorithm RNA22. [score:3]
Next, we tested the effect of antimiR knockdown of miR-410-5p on HFD -induced cardiac fibrosis. [score:2]
In summary, our findings reveal that miR-410-5p acts as an endocrine regulator to promote metabolic disorders -mediated cardiac remo deling. [score:2]
Thus, obesity promotes cardiac fibrosis, at least in part, by regulating the miR-410-5p/TGFβ signaling. [score:2]
In contrast, the mutation abrogated the reduction of the luciferase activity in response to miR-410-5p (Fig.   5c). [score:2]
Unlike miR-410-3p, little is known about the physiological function of miR-410-5p. [score:1]
For constructing of Smad 7-3′UTR (Mut) reporter, the putative miR-410-5p binding site was replaced with the sequence as shown below (Mut). [score:1]
Our results reveal that the levels of miR-410-5p are markedly higher in exosomes of rats fed HFD than in control rats. [score:1]
More recently, these authors have reported that the miR-410-5p can degrade the miR-410-3p through base pairing to form a duplex between the two miRNAs in DCs [34]. [score:1]
H9c2 cells were cultured in 24-well plates were transfected using Lipofectamine 2000® Reagent (Thermo Fisher Scientific) with 0.25 μg of the vector as well as rno-miR-410-5p mimics. [score:1]
miR-410 belongs the largest known mammalian miRNA cluster, the Gtl2-Dio3 noncoding RNA locus [30]. [score:1]
To confirm this point, we detected pre-miR-410 in major organs, such as liver, heart, kidney, muscle and adipose tissues using qPCR. [score:1]
After fed HFD for 21 weeks, the rats were injected once weekly for three consecutive weeks with miR-410-5p antimiR. [score:1]
The rats were infected with lentivirus particles containing PGLV3-miR-410 or PGLV3-miR-410-5p antimiR or PGLV3-NC was co -transfected with three other helper plasmids (PG-P1-Gag- VSVG, PG-P2-REV, and PG-P3-RRE) into human embryonic kidney 293 T cells. [score:1]
ROC curve analysis has shown that miR-410-5p was a specific diagnostic biomarker of prostate cancer. [score:1]
miR-410-5p promotes cardiac fibrosis. [score:1]
Rats fed HFD for 21 weeks were injected with 1 × 10 [8] TU of lentivirus particles containing PGLV3-miR-410-5p antimiR or PGLV3-NC through tail vein injection. [score:1]
The rats were infected with lentivirus particles containing PGLV3-miR-410 or PGLV3-NC. [score:1]
We found that miR-410-5p antimiR attenuated cardiac fibrosis, and restored the protein levels of Smad 7 in rats fed HFD (Fig. S3a,b). [score:1]
miR-410-5p from the kidney and adipose tissues probably induces cardiac fibrosis. [score:1]
The exosomal miR-410-5p is then transferred to the recipient tissue heart. [score:1]
As expected, injection of rats with PGLV3-miR-410 led to a decrease in the protein levels of Smad 7 and an increase in the phosphorylation levels of Smad 2 (Fig.   6a,b). [score:1]
Figure 8 A proposed mechanism of miR-410-5p -induced cardiac fibrosis in rats with obesity. [score:1]
We found that the levels of miR-410-5p in exosomes of rats fed HFD were markedly higher than those in control rats (Fig.   7d). [score:1]
To test this hypothesis, we first examined the levels of miR-410-5p in the serum, and found that the miR-410-5p levels were notably elevated in the serum of rats fed HFD (Fig.   7c). [score:1]
When 60–80% confluent, the cells were transfected using Lipofectamine 2000® Reagent (Thermo Fisher Scientific, Waltham, MA) with 0.25 μg of the negative control or rno-miR-410-5p mimics: 5′-Agguugucugugaugaguucg-3′ labeled with 2′-Ome (obtained from GenePharma Company, Shanghai, China). [score:1]
We thus isolated exosomes from serum and determined the levels of miR-410-5p using qPCR. [score:1]
Our results revealed that the levels of pre-miR-410 in the kidney and adipose tissues were 16~40-fold higher than those in the liver, heart, and muscle tissues (Fig.   7a). [score:1]
miR-410-5p antimiR (5′-CGAACUCAUCAGAGACAACC-3′) was inserted into the lentivirus vector PGLV3/H1/GFP + Puor vector (PGLV3), resulting in the vector PGLV3-miR-410-5p antimiR. [score:1]
In this report, we have demonstrated that miR-410-5p is involved in cardiac fibrosis, an important part of cardiac remo deling, in rats fed HFD. [score:1]
The titers of the PGLV3-miR-410 or PGLV3-NC vectors were 1 × 10 [9] transfer units (TU/ml). [score:1]
Similarly, the protein levels of CTGF, collagen-II, and collagen-IV were also increased in miR-410-5p -treated heart (Fig.   6e,f). [score:1]
In brief, pre-miR-410 (5′-ACTTGAGGAGAGGTTGTCTGTGATGAGTTCGCTTT ATTAATGACGAATA TAACACAGATGGCCTGTTTTCAATACC-3′) was inserted into the lentivirus vector PGLV3/H1/GFP + Puor vector (PGLV3), resulting in the vector PGLV3-pre-miR-410. [score:1]
A recent study from Wang et al. has demonstrated that circulating miR-410-5p levels are significantly elevated in the patients with prostate cancer [33]. [score:1]
Importantly, miR-410-5p is conserved miRNA among many species including human and rodents (Fig.   5b). [score:1]
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[+] 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-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-25, 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, 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
These candidate miRNAs included representatives that exhibited regulated patterns of expression from each of the two primary classes detected, namely: those with highest expression in the caput (let-7c-5p, let-7b-5p, miR-375-3p, miR-9-5p, miR-467d-3p, and miR-200c-3p), or highest expression in the cauda (miR-410-3p, miR-486-5p, and miR470c-5p) epididymis. [score:8]
0135605.g008 Fig 8In order to verify the next generation sequence data, nine differentially expressed miRNAs were selected for targeted validation using qRT-PCR, including representatives with highest expression in the proximal (caput: let-7c-5p, let-7b-5p, miR-375-3p, miR-9-5p, miR-467d-3p, and miR-200c-3p) and distal (cauda: miR-410-3p, miR-486-5p, and miR470c-5p) epididymis. [score:7]
In order to verify the next generation sequence data, nine differentially expressed miRNAs were selected for targeted validation using qRT-PCR, including representatives with highest expression in the proximal (caput: let-7c-5p, let-7b-5p, miR-375-3p, miR-9-5p, miR-467d-3p, and miR-200c-3p) and distal (cauda: miR-410-3p, miR-486-5p, and miR470c-5p) epididymis. [score:7]
Only miR-410-3p failed to present significant changes in expression, however this result may be attributed to the relatively low absolute expression of this miRNA (Fig 8). [score:5]
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[+] score: 9
Other miRNAs from this paper: hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-139, hsa-mir-181c, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-140, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-296, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, hsa-mir-324, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-15b, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-19a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-129-1, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-181c, rno-mir-186, rno-mir-204, rno-mir-212, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, rno-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-181d, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-381, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Finally, other subsets of miRNAs were either up-regulated (miR-23a-3p, miR132-3p, miR-146a-5p, miR-154-3p, miR-181d-5p, miR-212-3p, miR-212-5p, miR-344b-5p, miR-380-3p, miR-410-3p, miR-433-3p and miR-3584; Fig. 2, Supplementary Fig. S4), or down-regulated (miR-29c-5p, miR-30a-5p, miR-30c-2-3p, miR-30e-3p, miR-138-5p, miR-140-3p, miR-551b-3p and miR-652-3p; Fig. 2, Supplementary Fig. S5) during all phases of the disease. [score:9]
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[+] score: 8
miR-410-3p is known to directly target lactate dehydrogenase A (LDHA), a gene selectively repressed in normal insulin secreting b-cells. [score:4]
Human embryonic stem cells (hESCs) can be induced to express miR-410, keeping LDHA levels in check, which were then differentiated in vitro into pancreatic endoderm (Safdar and Tarnopolsky, 2017). [score:3]
miR-410 enhanced hESC-derived pancreatic endoderm transplant to alleviate gestational diabetes mellitus. [score:1]
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[+] score: 5
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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[+] score: 4
In the chronic liver injury mo dels including the HFD, MCDD, and CCl [4] groups, we found that 3 miRNAs (miR-10b*, miR-410, miR-499) were commonly down-regulated, but were not affected in the acute liver injury mo dels (Fig. 4), suggesting that these miRNAs might serve as biomarkers of steatosis. [score:4]
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[+] score: 3
miR-379, miR-410, and 16 other miRNAs from this subcluster were among the 2-week-specific miRNAs in our study and were present in k-means clusters 2 or 3. Their association with neonatal energy homeostasis is consistent with their expression at 2 weeks of age, when animals are transitioning from maternal energy sources to independent feeding. [score:3]
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[+] score: 1
Other miRNAs from this paper: hsa-mir-410
Moreover, it was showed that RPE cells could differentiate from MSCs using anti-miR-410 treatment without use of additional factors [37]. [score:1]
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[+] score: 1
In contrast at 7d, rno-miR-873 (degree of 55), rno-miR-223 (degree of 48) and miR-410 (degree of 45) had the highest degrees of connectivity. [score:1]
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