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27 publications mentioning rno-mir-378a

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-378a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 158
Other miRNAs from this paper: rno-mir-125a, rno-mir-378b
Both the expressions of TUSC-2 and TNFα were downregulated in miR-378 -transfected MSCs under a hypoxic environment, implicating that miR-378 may relieve hypoxia -induced apoptosis via downregulating TUSC-2 and TNFα. [score:9]
In the miR-378 group, TNFα protein expression was decreased under the normoxic environment (Figure  4B) and its expression was downregulated both on mRNA and protein level in hypoxic conditions (Figure  4B, E). [score:8]
The expression of proapoptosis genes was decreased whereas angiogenesis-related genes were found to be upregulated after miR-378 transfection. [score:6]
There was no difference of the expression of BCL2 between the miR-378 group and the control group under normoxic and hypoxic environments (Figure  4A, C), whereas BAX expression was reduced in the miR-378 group under a hypoxic environment (Figure  4A, D). [score:5]
The expression of the miR-378/miR-378 hairpin enhances cell survival through targeting the transcription factor SuFu and Fus-1 [21]. [score:5]
In the miR-378 group, there was no alteration of the expression of BCL2 both under the normoxic and hypoxic conditions, while the BAX level was decreased in the hypoxic condition, implying that miR-378 could attenuate the apoptosis of MSCs via suppressing the proapoptosis genes of the BCL2 family. [score:5]
miR-378 expression status after transfection with miR-378 mimic was confirmed by quantitative RT-PCR (P < 0.01; Figure  1A) The two experimental groups presented a lower growth and proliferation rate under a hypoxic environment at 72 hours and 96 hours, while both groups showed a higher inhibition rate in this condition (P < 0.01; Figure  1B, C, D). [score:5]
miR-378 binds to the 3′ untranslated region of VEGF to compete with miR-125a for the same seed region and strengthens VEGF expression [45]. [score:5]
miR-378 may reduce hydrogen peroxide and hypoxia -induced cell death by suppressing the expression of IGF-1R and its downstream AKT signaling cascade [24]. [score:5]
Evidence has revealed that miR-378 improves cell survival and inhibits apoptosis via regulation of various signaling networks and apoptosis-related genes [24]. [score:4]
Moreover, miR-378 is capable of reducing the expression of TUSC-2 at the protein level [21]. [score:3]
In this study, VEGFα expression was found to be declined in the control group after hypoxia exposure and this alteration could be mitigated after miR-378 transfection. [score:3]
The inhibition rate of the miR-378 group was lower under a hypoxic environment at 72 hours and 96 hours (3.73% vs. [score:3]
The miR-378 expression level was quantified using probes for miR-378 and U6 RNA (internal control). [score:3]
Expression of angiogenesis-related genes was enhanced after miR-378 transfection. [score:3]
Further explorations of the implications of miR-378 on MSCs in vivo will provide new mentalities for the treatment of ischemic heart disease based on MSCs transplantation. [score:3]
A distinct reduction of miR-378 in patients with heart failure has been reported, implying that it may also participate in the disease progression of heart failure [26]. [score:3]
Figure 5 microRNA-378 enhanced the expression of angiogenesis-related genes. [score:3]
BAX expression was reduced in the miR-378 group under the hypoxic environment. [score:3]
miR-378 is involved in the expression of VEGF [45]. [score:3]
In this study, we found that miR-378 transfection notably intensified the expression of TGFβ1, which could play a crucial role in promoting MSC differentiation into blood vessels. [score:3]
To obtain MSCs overexpressing miR-378 effectively, third-passage MSCs were transfected with miR-378 mimic using Lipofectamine™ 2000 (catalogue number 11668019; Invitrogen, Carlsbad, California, USA) according to the manufacturer’s instructions. [score:3]
Expression of apoptosis-related genes was decreased after miR-378 transfection. [score:3]
In addition, VEGFα expression was increased at the protein level in the miR-378 group in hypoxic conditions. [score:3]
However, no differences in their expressions were observed in the miR-378 group when exposed to the same environment (Figure  5). [score:3]
showed that the expression of VEGFα, PDGFβ and TGFβ1 was increased in miR-378 transfected MSCs under both normoxic and hypoxic conditions (Figure  5A). [score:3]
In the present work, PDGFβ was increased in MSCs transfected with miR-378 under normoxic and hypoxic conditions, indicating that miR-378 might improve PDGF expression in this condition. [score:3]
13.60%, P < 0.01) (Figure  1D), indicating that miR-378 could alleviate the inhibition of MSC proliferation induced by hypoxia–ischemia. [score:3]
Experimental studies show that miR-378 transfection significantly enhances cell viability and inhibits cell apoptosis [22, 23]. [score:3]
In the miR-378 group, there was a decreased expression of tumor necrosis factor-α on protein level and a reduction of TUSC-2 under normoxic environment. [score:3]
Figure 4 microRNA-378 decreased the expressions of apoptosis-related genes. [score:3]
Its level was downregulated in the miR-378 group compared with the control group under normoxic and hypoxic environments (Figure  4B, F). [score:3]
microRNA-378 (miR-378) is a specific miRNA that can induce angiogenesis in tumors [21]. [score:1]
miR-378 might function on apoptosis-related and angiogenesis-related genes. [score:1]
Native MSCs, MSCs cultured in normoxic conditions; miR-378, miR-378 -transfected MSCs cultured in normoxic conditions; MSCs + hypoxia, MSCs cultured in hypoxic conditions; miR-378 + hypoxia, miR-378 -transfected MSCs cultured in hypoxic conditions. [score:1]
miR-378 mimic (mature sequence rno-miR-378a-5p: 4-cuccugacuccagguccugugu-25) was synthesized and provided by Ruibo Biotechnology Corporation (Guangzhou, China). [score:1]
Both PDGFβ and TGFβ1 were discovered to be increased in MSCs transfected with miR-378. [score:1]
Figure 1 Mesenchymal stem cell proliferation after the transfection of microRNA-378. [score:1]
Examination of the apoptosis of MSCs showed that the number of terminal deoxynucleotidyl transferase biotin-dUPT nick end-labeling -positive cells was significantly decreased in the miR-378 group. [score:1]
lane a, DAPIr staining localization; lane b, TUNEL staining; lane c, overlap figure of lanes a and b. (B) Comparison of apoptotic rates between groups after miR-378 transfection in normoxic and hypoxic environments. [score:1]
The miR-378 group displayed a more rapid growth under hypoxic environment at 72 hours and 96 hours in contrast with the control group (0.78 ± 0.02 vs. [score:1]
Cell apoptosis percentage in the miR-378 group was significantly declined under normoxic and hypoxic condition (0.30 ± 0.10% versus 0.50 ± 0.10%, P <0.05; 0.60 ± 0.40% versus 1.70 ± 0.20%, P <0.01). [score:1]
In the present study, we demonstrated that MSCs transfected with miR-378 formed a larger number of vascular branches on matrigel, indicating that miR-378 could enhance the capability of MSCs differentiation into vascular lineage. [score:1]
Once cocultured with human umbilical vein endothelial cells, MSCs transfected with miR-378 formed a larger number of vascular branches on matrigel. [score:1]
In summary, this study showed that miR-378 could promote MSCs survival and the cells’ ability of vascularization under hypoxic–ischemic conditions in vitro. [score:1]
Figure 3 microRNA-378 promoted the angiogenesis ability of mesenchymal stem cells. [score:1]
The miR-378 group formed a larger number of vascular branches on matrigel. [score:1]
Cells transfected with miR-378 showed more rapid growth and a higher proliferation rate after 24 hours of hypoxia/reoxygenation. [score:1]
Hypoxia -induced apoptosis in MSCs was alleviated after miR-378 transfection. [score:1]
miR-378 microRNA-378 miRNA microRNA MSC mesenchymal stem cell PDGF platelet-derived growth factor RT-PCR real-time polymerase chain reaction TGFβ1 transforming growth factor beta-1 TNFα tumor necrosis factor alpha VEGF vascular endothelial growth factor. [score:1]
In this study, MSCs were transfected with miR-378 and exposed to normal and hypoxic–ischemic conditions to observe their survival, proliferation and apoptosis. [score:1]
How miR-378 could act on MSCs survival and differentiation in the injured heart in animal mo dels would be further explored in our later work. [score:1]
MSCs without transfection were applied as the negative control; experiments using scrambled miRNA as a control for the miR-378 transfection would further be performed to eliminate nonspecific effects of transfection and make the data more convincing. [score:1]
The present study demonstrates that MSCs transfected with miR-378 showed higher viability and a lower apoptosis rate under hypoxic–ischemic conditions. [score:1]
The results indicated that MSCs could be efficiently transfected with miR-378 without affecting cells viability. [score:1]
The third passage of MSCs were divided into the miR-378 group and control group. [score:1]
miR-378 is closely associated with stem cell survival and vascular differentiation. [score:1]
For the miR-378 group, cells were transfected with miR-378 mimic. [score:1]
Angiogenesis ability of MSCs was promoted after miR-378 transfection. [score:1]
Mesenchymal stem cells survival was enhanced post transfection of miR-378. [score:1]
In addition, miR-378 is a newly described member of the cardiac-enriched miRNAs modulating cardiac growth during the postnatal period [24]. [score:1]
microRNA-378 transfection. [score:1]
Previous studies have confirmed that miR-378 plays an important role in blood vessel formation [40, 41]. [score:1]
As this study was conducted in vitro, the affection of miR-378 on MSCs in vivo is still lacking. [score:1]
Prior studies have demonstrated that miR-378 facilitates cancer cell migration and promotes their survival [21]. [score:1]
Under normoxic conditions, the numbers of vascular branches in the miR-378 group were obviously higher than in the control group (17.50 ± 0.55 vs. [score:1]
Twenty-four hours after transfection, cells of the miR-378 group (MSCs transfected with miR-378) and the control group (MSCs without transfection) were both incubated in serum-free media with 1% oxygen in a Galaxy® 48 R incubator (Eppendorf/Galaxy Corporation, Connecticut, USA) at 37°C for 24 hours and then exposed to normoxic conditions (20% oxygen) for another 24 hours. [score:1]
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[+] score: 20
Analysis at P21 revealed 74 mature miRNAs with differential expression between LPD -induced IUGR rat lungs and control lungs (Fig 1): 10 showed more than twofold differential expression: miR-184, miR-127-3p, miR-378a-5p and miR541-5p were downregulated, and miR-30e-5p, miR-23b-5p, miR-451-5p, miR-1839-5p, miR-449a-5p, and miR-19b-3p were upregulated in LPD -induced IUGR versus control lungs. [score:11]
At P21, the differential expression of 5 of 10 of the miRNAs was statistically confirmed, with miR378a-5p, miR127-3p, and miR184 downregulated and miR30e-5p and miR449a-5p upregulated. [score:9]
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[+] score: 18
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]
Moreover, miR-378a-3p has been shown to suppress the activation of HSCs by targeting Gli3, and injection of miR-378a-3p mimics into mice was shown to ameliorate chronic liver injury induced by CCl [4] [18]. [score:5]
Hyun J MicroRNA-378 limits activation of hepatic stellate cells and liver fibrosis by suppressing Gli3 expressionNat. [score:4]
For example, Tu et al. [33] reported that lentivirus -mediated ectopic expression of miR-101 in liver greatly reduced CCl [4] -induced liver fibrosis and Hyun et al. [18] showed that systemic delivery of miR-378a-3p by nanoparticle technology significantly reduced hepatic damage. [score:3]
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[+] score: 16
Consistent with previous research [36, 38], our results suggest that upregulation of miR-21-5p and miR-378-3p mitigated hypoxia -induced apoptosis and enhanced cell viability, thereby supporting adaptation of the cell to the hypoxic conditions. [score:4]
Similarly, upregulation of miR-378-3p robustly mitigated hypoxia -induced cell damage (Figure S2A–E). [score:4]
These results demonstrate that miR-152-3p and let-7i-5p resemble miR-21-5p and miR-378-3p, which are highly expressed in hypoxic H9c2 cells-derived exosomes, and have anti-apoptotic and pro-viability effects in H9c2 cells under hypoxic stress. [score:3]
To further investigate the biological function of hypoxia -induced exosomal miRNAs in H9c2 cell apoptosis, we selected miR-21-5p, miR-378-3p, miR-152-3p, and let-7i-5p, which were significantly upregulated in hypoxic exosomes and participated in apoptosis, for functional verification. [score:2]
Among these miRNAs, miR-21-5p, and miR-378-3p have been reported to have anti-apoptotic effects in cardiomyocytes under hypoxic stress [36, 37]. [score:1]
Interestingly, we found that some exosomal DE miRNAs, including miR-21-5p, miR-378-3p, miR-152-3p, and let-7i-5p, had potential anti-apoptotic and pro-viability effects in H9c2 cells under hypoxic stress. [score:1]
Based on our small RNA-seq results and bioinformatic prediction, we selected several miRNA to use to verify function, including miR-21-5p, miR-378-3p, miR-152-3p, and miR-let-7i-5p. [score:1]
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[+] score: 16
Co -expression of miR-34a with miR-19a, miR-378, or miR-326 did not modulate the inhibition induced by miR-34a expression alone. [score:7]
Inhibition of the Arc 3′UTR by miR-326 was not affected by co-transfection with miR-19a, yet significantly stronger inhibition was obtained when miR-326 was paired with miR-193a or miR-378. [score:5]
For further validation we selected the four miRNAs (miR-34a, miR-193, miR-378, and miR-512-5p) with strongest inhibitory effect on the Arc 3′UTR. [score:3]
miR-378 and miR-34a also have a synergistic effect yet bind to quite wi dely separated (1000 nt) sites. [score:1]
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[+] score: 14
Therefore, increased expression of miR-29 and miR-24 and reduced expression of miR-34, miR-130 and miR-378 may be responsible for the beneficial effects exerted by MSC-Exo. [score:5]
Moreover, the low expression of miR-130 and miR-378 in both MSC-Exo and MSCs found in our study is in line with other reports that high expression of the miR-130 and miR-378 caused K ion channel dysfunction in cardiac stem cell and cardiac hypertrophy [37, 38]. [score:5]
We found that the expression of miR-130, miR-378, and miR-34, which negatively regulate cardiac functions, was relatively low. [score:4]
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[+] score: 14
Our previous studies found that miR-378 inhibited caspase-3 expression and attenuated ischemic injury in cardiomyocytes [6], and that miR-199a might be a potential therapeutic target for cardiac hypertrophy or heart failure [7]. [score:7]
00191.2012 22942181 6. Ji F Overexpression of microRNA-378 attenuates ischemia -induced apoptosis by inhibiting caspase-3 expression in cardiac myocytesApoptosis. [score:7]
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[+] score: 13
Other miRNAs from this paper: rno-mir-21, rno-mir-34a, rno-mir-127, rno-mir-378b
For example, up-regulated miR-21 was reported to be involved in regulating the proliferative phase of LR by targeting Pellino-1 (Peli1) [8] and B-cell translocation gene 2 (Btg2) [9], Down-regulated miR-378 has a regulatory role by inhibiting DNA-synthesis-promoting gene ornithine decarboxylase (Odc1) during the early phase of LR [9]. [score:13]
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[+] score: 11
For example, miR-378 targets the 3′-UTR of Igf1r, Grb2, Ksr1, and Mapk1 to regulate the mitogen-activated protein kinase (MAPK) pathway [9]. [score:4]
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]
For example, it has been reported that Igf1r is a target of miR-1 [55], miR-139 [56], miR-378 [57], miR-99a [58], and miR-497 [59]. [score:3]
Our cardiac-specific GSA recapitulated the previously known miRNA-pathways, including miR-486 in PI3K-Akt signaling (p-value: 1.59E-03) [24], miR-17–92 in TGF-β signaling (p-value: 6.34E-03) [54] and miR-378 in MAPK signaling (p-value: 1.76E-02; S2 Table) [9]. [score:1]
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[+] score: 9
Three miRNAs profiles were found with (A) rno-miR-133b-3p, rno-miR-378a-3p, and rno-miR-434-3p equally expressed in both muscle types, (B) rno-miR-1-3p and rno-miR-133a-3p with higher expression in EDL and (C) rno-miR-206-3p, mmu-miR-208b-3p, and rno-miR-499-5p with higher expression in SOL. [score:7]
Three miRNAs profiles were found with (A) rno-miR-1-3p and rno-miR-133a-3p rising in response to both SOL and EDL muscle damage, (B) rno-miR-133b-3p, rno-miR-378a-3p, and rno-miR-434-3p with higher levels following EDL muscle damage and (C) rno-miR-206-3p with higher levels following SOL muscle damage. [score:1]
In healthy organisms, our group demonstrated that exercise -induced muscle damage (EIMD) in human, as well as toxic muscle injury in rats, induced an early elevation of a subset of muscle specific (miR-1, -133a, 133b, -206, -208b, -499) and non-muscle specific miRNAs (miR-378a, -434) (Banzet et al., 2013; Siracusa et al., 2016). [score:1]
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[+] score: 7
In the mo del group, 17 miRNAs were downregulated, including miR-1, miR-133, miR-29, miR-126, miR-212, miR-499, miR-322, miR-378, and miR-30 family members, whereas the other 18 miRNAs were upregulated, including miR-21, miR-195, miR-155, miR-320, miR-125, miR-199, miR-214, miR-324, and miR-140 family members. [score:7]
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[+] score: 6
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-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-22, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-101a, mmu-mir-126a, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-142a, mmu-mir-181a-2, mmu-mir-194-1, hsa-mir-208a, hsa-mir-30c-2, mmu-mir-122, mmu-mir-143, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-208a, 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-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29c, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-20a, rno-mir-101b, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-17, mmu-mir-19a, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-19b-1, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, 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-18a, rno-mir-19b-1, rno-mir-19a, rno-mir-22, rno-mir-26a, rno-mir-26b, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30c-2, rno-mir-98, rno-mir-101a, rno-mir-122, rno-mir-126a, rno-mir-130a, rno-mir-133a, rno-mir-142, rno-mir-143, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-208a, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-499, hsa-mir-378d-2, mmu-mir-423, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-29c-2, rno-mir-1b, ssc-mir-26b
miR-101, miR-378 and 143 expression patterns. [score:3]
The expression of miR-378 was highly variable among the tissues tested (Figure 2E). [score:3]
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[+] score: 6
For example, microRNA-378 limited the activation of HSCs and liver fibrosis by regulating expression of its target glioma -associated oncogene family zinc-finger 3 gene [10]. [score:6]
[1 to 20 of 1 sentences]
[+] 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: 5
In order to validate the changes in miRNA expression detected by a deep-sequencing, we conducted quantitative real-time PCR analysis to examine expression levels of six miRNAs including rno-miR-378, rno-miR-182, rno-miR-21, rno-miR-34a, rno-miR-34b, and rno-miR34c. [score:5]
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[+] score: 5
A number of miRNAs have been reported to target caspase-3. miR-378 has been reported to attenuate apoptosis of cardiomyocytes by targeting caspase-3 [33]. [score:5]
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[+] score: 4
To better elucidate the mechanism between miR-208 and myocardial I/R injury, we performed the experiments described in this report according to some of the methods reported by Fang et al. [17], who used a miR microarray to analyze an in vivo rat mo del of 4-h myocardial ischemia without reperfusion and found that miR-378 overexpression conveyed a protective role to cardiomyocytes following ischemic injury. [score:3]
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: 4
Other miRNAs have been implicated in various kidney diseases, including in renal fibrosis (miR-22) [49], nephritic syndrome (miR-181a) [50], and renal cell carcinoma (miR-378) [51]. [score:3]
Levels of miR-191 and miR-378 were elevated in the urine of rats dosed with nephrotoxicants [52, 53]. [score:1]
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[+] score: 3
Specifically, some studies have focused on the roles of miRNAs in the protective effects of fish oil or omega-3 PUFAs against metabolic syndrome and found that the intake of fish oil or DHA/EPA can modify the expression of miR-30b and miR-378 [49], miR-33a and miR-122 [50], miR-107 [51], miR-192, and miR-30c [52]. [score:3]
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[+] score: 3
Out of the 14 miRNAs that were detected to be differentially expressed using NGS (Table  4), five (rno-let-7d-5p, rno-miR-100-5p, rno-miR-203a-3p, rno-miR-21-5p, rno-miR-320-3p) were represented on the TLDA-A, while nine (rno-miR-378a-3p, mmu-miR-5100, rno-miR-30e-3p, rno-miR-125b-2-3p, rno-miR-320-5p, rno-miR-3473, rno-miR-21-3p, rno-miR-455-5p, and hsa-miR-7641) were not. [score:3]
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Compared to the other 2 groups, 21 miRNAs are upregulated in 6-hour group as shown in the upper portion of Fig. 2, miR-9, miR-204, miR-335, miR-23a, miR-708, miR-146a, miR-325-5p, miR-106b, miR-143, miR-140, miR-376b-3p, miR-7a, miR-541, miR-185, miR-499, miR-127*, miR-320, miR-140*, miR-145*, miR-423*, miR-378. [score:3]
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miR-497, miR-218a, miR-378 and miR-503 were reported to have anti-carcinogenic effect in breast, glioma, liver, endometrial and gastric cancers respectively. [score:1]
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However, miR-378 (Fig. 4G) and the cardiac muscle-enriched miR-133a are exceptions. [score:1]
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In addition, the neural progenitor cells isolated by LCM exhibited increases in miR-146a, miR-146b, miR-210, miR-19b and miR-378 and decreases in miR-128, miR-291a-3p, and miR-139-5p (Fig. 3A to 3C), which are consistent with the array data findings. [score:1]
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5 mmu-miR-214 -1.7 -6.1 -10.9 mmu-miR-137 -31.7 -6.8 -144.8 mmu-miR-29c -1.8 -10.5 -10.7 rno-miR-532–5p -2.0 -59.1 -126.9 mmu-miR-466d-3p -2.7 -4.2 -9.9 mmu-miR-466d-5p -23.2 -64.7 -105.7 mmu-miR-22 -1.6 -4.6 -9.9 mmu-miR-582–5p -21.3 -59.4 -97.1 mmu-miR-690 -1.9 -2.1 -9.7 rno-miR-421 -21.3 -59.3 -97.0 mmu-miR-193 -4.9 -3. 5 -8.1 mmu-miR-369–5p -20.9 -58.3 -95.3 mmu-miR-27b* -2.1 -2.9 -8.0 mmu-miR-684 -20.8 -58.1 -94.9 mmu-miR-378 -1.6 -4.6 -7.7 mmu-miR-375 -20.6 -57.6 -94.2 mmu-miR-9* -1.9 -18.4 -7.7 mmu-miR-337–5p -20.5 -57.4 -93.8 mmu-miR-204 -2.5 -5.3 -7.5 mmu-miR-15a* -20.3 -56.8 -92.8 mmu-miR-28* -1.9 -3.2 -6.5 mmu-miR-532–5p -19. [score:1]
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MicroRNA-378 alleviates cerebral ischemic injury by negatively regulating apoptosis executioner Caspase-3. Int. [score:1]
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Other miRNAs from this paper: rno-mir-328a, rno-mir-17-1, rno-mir-17-2, rno-mir-328b, rno-mir-378b
B, RT-PCR of mature miR-328, miR-378, miR-17-3p, and miR-17-5p using RNA prepared from A431 cells stably transfected with miR-328 and a control vector, confirming that processing of other microRNAs was not affected by miR-328 transfection. [score:1]
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