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14 publications mentioning rno-mir-377

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-377. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 227
miR-377 mimic and its negative control (NC) (miRIDIAN Mimic, Thermo Scientific), miR-377 inhibitor and its negative control (miRCURY LNA microRNA inhibitor, Exiqon), VEGF siRNA and its negative control(ON-TARGET plus SMARTpool, rat VEGF-A, Thermo Scientific) were assigned into 6 groups for transfection as follows: A. miR-377 mimic (miR-377); B. Negative control (NC)-miR-377 -mimic (NC [miR]); C. miR-377 inhibitor (Anti-377); D. NC-miR-377 -inhibitor (NC [Anti-377]); E. VEGF siRNA; F. NC-VEGF siRNA (NC [siRNA]). [score:11]
Elevation of miR-377 in MSCs suppressed VEGF expression at both mRNA and protein levels (by ∼70%) in Fig. 4A and 4B, which conversely were upregulated by ∼2.5-fold in miR-377-knockdown MSCs (Anti-377) (Fig. 4Aand 4B). [score:9]
0104666.g004 Figure 4(A): qPCR analysis after normalization against β-actin showed that miR-377 mimic (miR-377) downregulated VEGF mRNA in MSCs, while miR-377 inhibitor (Anti-377) upregulated VEGF mRNA in MSCs. [score:9]
When the signal density of miRs was cut off by a value of 100, a group of 13 miRs were significantly up-regulated including miR-210, -25, -450a, -130a, -3593-3p, -34c*, -214, -181a, -23b, -34a, -31, -31*, and -140*; whereas 20 miRs (miR-377, -146a, -222, -652*, -466b-1*, -664-1*, -196c*, -466c*, -29c, -32*, -195, -466b, -188, -146b, -92a, let-7b, -466b-2*, -466d, -485*, and -181c) were significantly down-regulated in MSCs under hypoxic conditions. [score:7]
MSCs were harvested 48 hours after transfection with either NC-miR (NC [miR]), NC-Inhibitor (NC [Anti]), miR-377 mimic (miR-377), or miR-377 inhibitor (Anti-377) to ascertain if miR-377 modulates VEGF expression. [score:7]
Lenti-GFP, lentiviral empty vector; Lenti-miR-377, lentiviral miR-377 overexpressing vector; Lenti-Anti-miR-377, lentiviral miR-377 inhibitor expression vector. [score:7]
MiR-377 and miR-210 are the most significantly dysregulated miRs in hypoxia -treated rat MSCs compared to normoxia -treated MSCs (the green stands for down-regulation, and the red stands for upregulation). [score:7]
Computational miRNA target prediction analysis was performed to elucidate the potential mechanism of miR-377 in the regulation of angiogenesis, using TargetScan and miRDB. [score:6]
These results indicate that enhanced effects in the formation of tube-like structures induced by knockdown of miR-377 were abolished by inhibition of VEGF expression. [score:6]
Lentiviral Overexpression and Suppression of miR-377. [score:5]
miR-377 directly down regulates the expression of VRGF in MSCs. [score:5]
HUVECs were transiently transfected with A. negative control (NC [miR]/NC [Anti]); B. miR-377 mimic; C. miR-377 inhibitor; D. miR-377 inhibitor+VEGF siRNA. [score:5]
HUVECs were transfected with either miR mimic to overexpress miR-377 or miR inhibitor to specifically knockdown miR-377 (Fig. 2A) in order to determine the significance of miR-377 in angiogenesis, followed by an in vitro tube-formation assay using Matrigel-precoated wells. [score:5]
In conclusion, our study indicates thathypoxia-reducedmiR-377 directly targets VEGF, and knockdown of endogenous miR-377 promotes MSC transplantation -induced angiogenesis and subsequent heart function improvement post MI. [score:5]
By computational miRNA target prediction analysis, we identified VEGF as a potential target of miR-377. [score:5]
These findings suggest that miR-377 may serve as a novel potential therapeutic target for treatment of ischemic heart diseases. [score:5]
Therefore, our study indicates that miR-377 may be a novel therapy target for treatment of ischemic heart disease. [score:5]
Lentiviral vectors (pEZX-MR03) for overexpression and suppression of miR-377 (Null, miR-377, and Anti-377) were purchased from Genecopoeia Corp. [score:5]
Furthermore, both dual-luciferase reporter assay and Western-blotting verified that miR-377 can directly bind with VEGF 3′UTR leading to negatively regulation of its expression. [score:4]
miR-377 was the most down-regulated in MSCs upon hypoxia treatment (Fig. 1B). [score:4]
For the first time we demonstrate that miR-377 is responsive to hypoxia and directly targets VEGF in MSCs. [score:4]
Our results show for the first time that miR-377 was strongly down-regulated in hypoxia -treated MSCs, which was a major factor contributing to the increased VEGF levels. [score:4]
Engineering rat MSCs with lentiviral vectors to overexpress or knockdown of miR-377. [score:4]
Accordingly, in vivo by transplanting MSCs with genetic overexpression or knockdown of miR-377 in the rat MI hearts, we observed that myocardial angiogenesis was significantly improved in MSC [Anti-377] -treated hearts, whereas it was poor in MSC [miR-377] -treated hearts when comparable to MSC [Null] -injected hearts. [score:4]
Luciferase activity was repressed by 67% when miR-377 was co-expressed with the VEGF-3′-UTR luciferase reporter vector (Fig. 3C), whereas luciferase activity of mutated VEGF-3′-UTR was not affected. [score:3]
The expression of VEGF was knocked down in miR-377-reduced HUVECs by siRNA, followed by in vitro tube formation assay. [score:3]
It is important to determine whether miR-377 reduction-caused angiogenesis is dependent on VEGF given that VEGF is a target for miR-377. [score:3]
Reduced Expression of miR-377 in HUVECs Promotes Angiogenesis. [score:3]
VEGF-A (usually referred to as VEGF) is listed among the top of assumed targets for rno-miR-377 and the seed sequence of VEGF 3′UTR interacting with rno-miR-377 is highly conserved among the species of rat, human, chimpanzee, rhesus, bushbaby, treeshrew, and mouse (Fig. 3A). [score:3]
In contrast, HUVECs co -transfected with miR-377 inhibitor+VEGF siRNA exhibited sparse capillary-like structures in which the tube length and the number of tube branch points are similar to NC group (Fig. 5A and 5B). [score:3]
Suppression of miR-377 induced in vitro formation of capillary-like structures. [score:3]
MiR-377 Negatively Regulates VEGF Expression in MSCs and ECs. [score:3]
Rat MSCs were genetically engineered to overexpress or suppress miR-377 using lentiviral transduction (Fig. 6A) to investigate the functional significance of miR-377 in MSC -induced angiogenesis in ischemic hearts. [score:3]
Suppression of miR-377 in MSCs Enhances Angiogenesis in Ischemic Hearts. [score:3]
Dual-luciferase reporter assay validates that miR-377 directly targets VEGF. [score:3]
0104666.g003 Figure 3(A): Computational miRNA target prediction analysis coincidentally reveals that the fragment 5′-GAAUCAC-3′ of miRNA-377 pairs well with the fragment 5′-GUGAUUC-3′ located at the 1568–1574 nt of VEGF 3′ UTR, which is a highly conserved site (red fonts) in most of mammals (e. g. rat, human, chimpanzee, rhesus, bushbaby, treeshrew, mouse). [score:3]
MSCs transfected with a scrambled sequence according to miR-377 mimic and miR-377 inhibitor as negative control (NC [miR] and NC [Anti] respectively). [score:3]
However, the miR-377 inhibitor group (Anti-377 group) displayed the formation of full and dense cellular networks (Fig. 2B). [score:3]
Moreover, it is also unknown whether alteration of miR-377 expression affects MSC -induced angiogenesis in ischemic myocardial tissue. [score:3]
This was well correlative with the reduced expression of miR-377 (Fig. 1C). [score:3]
0104666.g002 Figure 2Suppression of miR-377 induced in vitro formation of capillary-like structures. [score:3]
Both in vitro and in vivo evidence presented in this study indicate that knockdown of endogenous miR-377 enhances MSC -mediated angiogenesis and recovery of cardiac function in infarcted myocardium. [score:2]
Similar to previous findings (Fig. 2), it was observed that miR-377 -inhibitor -transfected HUVECs had well-developed networks of capillary-like tubes, evidenced by a 1.5-fold increase of cumulative tube length and 1.45- fold increase of tube branch points, compared with NC [miR] cells. [score:2]
Knockdown of endogenous miR-377 enhances MSC -mediated myocardial angiogenesis in vivo. [score:2]
While miR-210 is well recognized to have pro-angiogenic property in vivo and in vitro [15], [17], it is unknown whether hypoxia-responsive miR-377 also regulates angiogenesis. [score:2]
The results showed that miR-377 expression was decreased by more than 2-fold in hypoxia -treated MSCs as compared with normoxic condition. [score:2]
Pro-angiogenic effects elicited by knockdown of miR-377 are largely dependent on VEGF. [score:2]
HEK293TN cells were transfected with a Dual-Luciferase reporter vector containing the 3′-UTR of VEGF or mutated 3′-UTR of VEGF fused downstream to the Luciferase coding sequence (Fig. 3B) along with miR-377 mimic or a NC (NC [miR]) to validate whether miR-377 directly recognizes the 3′UTR of VEGF. [score:2]
Accordingly, qPCR (Fig. 6D) and Western blot (Fig. 6E) showed that VEGF expression was significantly reduced in MSC [miR-377] when compared with MSC [Null], whereas it was significantly increased in the MSC [Anti-377]group. [score:2]
Injection of miR-377-knockdown MSCs into the rat infarcted hearts limits fibrosis and improves cardiac functions. [score:2]
Thus, injection of miR-377-knockdown MSCs into an infarcted myocardium reduced overall infarction size and improved contractile function by promoting angiogenesis. [score:2]
Reduced Expression of MiR-377 in MSCs Limits Fibrosis and Improves Contractile Function in Infarcted Hearts. [score:2]
qPCR confirmed that MSC [Anti-377] exhibited lower levels of miR-377, whereas MSC [miR-377] exhibited significantly higher levels of miR-377 than MSC [Null] (Fig. 6C). [score:1]
2×10 [6] MSC [Null], MSC [miR-377], or MSC [Anti-377] was then injected into the border zone of ischemic left ventricular (LV) wall at 10 min. [score:1]
This may be interpreted that myocardial angiogenesis is reduced in MSC [miR-377] -treated hearts, but not enough to affect MSC -induced beneficial effects on the reduction of fibrosis and improvement of function in infarcted hearts. [score:1]
MSC [miR-377]. [score:1]
The 293TN cells were assigned into three groups to be transfected with A. pEZX-MT01 vector; B. pEZX-MT01 vector+NC-miR-377 mimic; C. pEZX-MT01 vector+miR-377 mimic. [score:1]
The NC [miR], miR-377, Anti-377, NC [Anti-377] and VEGF siRNA were added at the final concentration (100 nM for each well) after mixing with DharmaFECT Duo Transfection Reagent (Thermo Scientific) according to the manufacturer’s instructions. [score:1]
The negative control (NC [miR] and NC [Anti]) groups exhibited some tube-like shapes and half-full cellular networks, while the miR-377 mimic group (miR-377 group) revealed less tube-like structures and hardly formed cellular networks (Fig. 2B). [score:1]
0104666.g005 Figure 5 In vitro Tube Formation Assay showed that total capillary tube lengths (A) and tube branch points (B) were significantly reduced by the VEGF siRNA transfection in miR-377-knockdown HUVECs. [score:1]
Nearly 100% of MSCs were infected with Lenti-GFP (MSC [Null]), Lenti-miR-377 (MSC [miR-377]), or Lenti-Off-miR-377 (MSC [Anti-377]) after 72-hour transduction, as indicated by GFP fluorescence (Fig. 6B). [score:1]
No morphological changes were found among MSC [Null], MSC [miR-377], and MSC [Anti-377]. [score:1]
Negative Effects of miR-377 in Angiogenesis are Largely Dependent on VEGF. [score:1]
MiR-377 Acts Directly at the 3′UTR of VEGF. [score:1]
Therefore, determination of the role of miR-377 in myocardial angiogenesis and its associated mechanisms could be of major significance for techniques aimed at regeneration of heart tissue. [score:1]
In addition, the number of tube branch point in miR-377 group (19.5±2.2) was less than that of negative controls (NC [miR]36.0±2.9; NC [Anti]38.0±3.0 respectively), and was significantly increased in Anti-377 group (55.0±3.5) (Fig. 2C). [score:1]
Capillary density was identified by Von Willebrand (vWF) staining (green; white arrows) in (D) MSC [Null] group, (E) MSC [miR-377] group and (F) MSC [Anti-377] group. [score:1]
In vitro Tube Formation Assay showed that total capillary tube lengths (A) and tube branch points (B) were significantly reduced by the VEGF siRNA transfection in miR-377-knockdown HUVECs. [score:1]
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[+] score: 36
The miR-217 is known to be involved in increased collagen production and the progression of diabetic nephropathy through the down-regulation of PTEN and the subsequent activation of Akt kinase, and similar Akt up-regulation can be achieved by TGF-β -induced miR-192 18. miR-377 is thought to regulate the expression of fibronectin, another ECM protein that is up-regulated in diabetic nephropathy. [score:13]
In kidney, miRs have been reported to play a role in podocyte development 14– 16, the pathogenesis of diabetic nephropathy 17– 19 and polycystic kidney disease 20. miR-192, miR-217 and miR-377 have been described to be up-regulated in diabetic mouse and mesangial cells treated with TGF-β or exposure to high-glucose ambience 17– 19. [score:7]
Taxol down-regulated miR-192, miR-217 and miR-377 in remnant kidney, while it up-regulated miR-15a by microarray (Figure 5B, C) and real-time PCR analyses (Figure 5D). [score:7]
Expression of miR-377 has been found to be up-regulated in various mouse mo dels of diabetic nephropathy and in cultured human and mouse mesangial cells subjected to a high-glucose ambience or treated with TGF-β1 19. [score:6]
The expressions of three miRNAs, miR-217, miR-192 and miR-377, were found to be consistently high, and they were decreased with low-dose paclitaxel treatment in all three different biological samples, ie cortices, isolated tubular cells and NRK52E cells. [score:3]
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[+] score: 26
Other miRNAs from this paper: rno-mir-327, rno-mir-338, rno-mir-127, rno-mir-210, rno-mir-465
The expression levels of miR-465 [*] and miR-377 [*] were the most significantly upregulated, while the expression levels of miR-327 and miR-338 were the most downregulated. [score:11]
miR-465 [*] and miR-377 [*] were selected as the most upregulated miRNAs, while miR-327 and miR-338 exhibited the most downregulated expression. [score:9]
In addition, miR-377 has been shown to be upregulated in diabetic nephropathy and lung tumors (27), and abundantly expressed in transdifferentiated neuronal progenitors (28). [score:6]
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[+] score: 21
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
qRT-PCR measurements confirmed that the expression of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377 and miRNA-96 was up-regulated and that of miRNA-122, miRNA-200b, miRNA-466b, miRNA-138, miRNA-214, miRNA-503 and miRNA-27a down-regulated in adrenals from 17α-E2 treated rats (Fig. 3 ). [score:7]
Real-time quantitative PCR measurements confirmed that the expression of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377 and miRNA-96 was up-regulated and that of miRNA-122, miRNA-200b, miRNA-466b, miRNA-138, miRNA-214, miRNA-503 and miRNA-27a down-regulated in adrenals from 17α-E2 treated rats. [score:7]
The levels of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377, and miRNA-96 were up-regulated, whereas miR-125b, miRNA-200b, miR-122, miRNA-466b, miR-138, miRNA-214, miRNA-503 and miRNA27a were down-regulated in response to 17α-E2 treatment. [score:7]
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[+] score: 15
In addition to transcriptional regulation, we confirmed the editing of known ADAR targets in rat, and discovered that, in addition to the known edited miRNAs, mir-377 is edited in rat brains. [score:4]
In addition to known editing targets, such as mir-376b, we also identified the brain-specific mir-377 that was hitherto unknown to be edited. [score:3]
Furthermore, we confirmed specific A to I editing in brain for mir-376a/b/c and identified mir-377 as a novel editing target. [score:3]
For mir-377 we designed circular probes of which the termini were complementary to the miRNA, leaving a gap on the edited site (RT-mir377: TTGTGTGATTCAaaacaagagaagaagtagatgtactagtgctgccacaacattaatcaagaAAAAGTTGCC) We applied 11 μg total RNA (biological sample) or 1 pmol (synthetic miRNAs). [score:1]
The first two bars describe results obtained from brain, the only tissue from which mir-377 was cloned. [score:1]
C) qPCR data for mir-377. [score:1]
To quantify the degree of editing we verified editing of mir-377 by qRT-PCR analysis (Figure 2B, C, Additional file 11, Table S3). [score:1]
Optimization qPCR for mir-377. [score:1]
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[+] score: 11
miR-377 was also found to be upregulated in diabetic nephropathy [35]. [score:4]
By contrast, miR-26b-5p, miR-199a-3p, miR-377–3p, miR-let-7f-5p, miR-200a-3p, miR-21–5p, miR-152–3p, and miR-192–5p expressions were repressed by SO diet consumption. [score:3]
Lower expressions of miR-10b-5p and miR-377–3p were also observed in adult pups of rats fed FO diet compared with SO, OO, and PO diets. [score:2]
miR-377 is also related to diabetic nephropathy [35]. [score:1]
Likewise, we observed a decrease in the expression of several hepatic miRNAs, namely miR-192–5p, miR-10b-5p, miR-377–3p, and miR-215 after FO compared with OO and PO diets and miR-21–5p and mir-26b-5p after FO compared with PO diets. [score:1]
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[+] score: 8
Moreover, miR-377 is up-regulated in human and mouse mesangial cells exposed to high-glucose levels and can lead to increased fibronectin production in DN [13], while miR-216a regulates the collagen type I alpha 2 gene through mechanisms involving inhibition of the RNA binding protein Ybx1 [26]. [score:7]
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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[+] score: 8
Other miRNAs from this paper: rno-mir-27a, rno-mir-29c-1, rno-mir-192, rno-mir-29c-2
In addition, downregulation of miR-29c reduces podocyte apoptosis and decreases ECM protein accumulation, both in vitro and in vivo 37. miR-377 is upregulated in human and mouse MCs exposed to HG and indirectly stimulates increased fibronectin protein production 38. [score:8]
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[+] score: 6
Increased expression of miR-377 is also thought to regulate the expression of fibronectin [19]. [score:6]
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[+] score: 4
Similar with our findings, Sun et al. [31] discovered that lncRNA NEAT1 and miR-377-3p had a vital function in non-small cell lung cancer by regulating the target E2F3. [score:4]
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[+] score: 3
org) revealed several miRNA that might interact with POMC mRNA untranslated region, including miR-488, miR-485, miR-384-3p, miR-383, miR-377, miR-485-5p and miR-181 (family). [score:3]
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[+] score: 3
Altered expression of miR-192 and miR-377 has also been reported in diabetic kidney glomeruli and diabetic nephropathy respectively [35], [36]. [score:3]
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[+] score: 2
control Function rno-miR-653-3p 37.56097561 Unknown rno-miR-3594-3p 9.31358885 Unknown rno-miR-483-3p 8.414634146 Anti-apoptotic oncogene, cardiovascular inflammation and remo delling rno-miR-92b-5p 8.096126255 Heart development and atrial fibrillation rno-miR-377-5p 4.84735544 Atrial fibrillation and structural remo delling rno-miR-341 4.764878049 Atrial fibrillation and TGF-β/Smad2/3 pathway rno-miR-21-3p 4.637785208 Cell proliferation and invasion. [score:2]
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[+] score: 1
Moreover, we observed a significant increase in miR-320a and in miR-377-5p in LV of HF-rats respectively in 7 days and 2 months MI-rats (Fig.   1F–G). [score:1]
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