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13 publications mentioning mmu-mir-532

Open access articles that are associated with the species Mus musculus and mention the gene name mir-532. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 144
As miR-532-3p is able to suppress ARC expression, we wondered whether miR-532-3p regulated DOX sensitivity in cardiomyocytes by targeting ARC. [score:8]
Taken together, we report here that the upregulated expression of miR-532-3p in cardiomyocytes exposed to DOX in vitro and in vivo is involved in DOX cardiotoxicity by targeting ARC. [score:8]
We found that miR-532-3p was upregulated and ARC was downregulated in cardiomyocytes administered with DOX. [score:7]
Enforced expression of ARC showed a strong inhibitory effect on mitochondrial fission (Figure 6a) and cell death (Figure 6b) in the presence of miR-532-3p. [score:5]
Reduced endogenous expression level of miR-532-3p inhibited DOX -induced mitochondrial fission and cell death. [score:5]
Further, we used the luciferase assay system to test whether miR-532-3p can influence the expression of ARC by directly targeting ARC 3′UTR (Supplementary Figure S4d). [score:5]
Chemically modified antisense oligonucleotides (antagomirs) were used to inhibit endogenous miR-532-3p expression. [score:5]
Knockdown of ARC attenuated this inhibitory effect on mitochondrial fission (Figure 6c) and cell death (Figure 6d) in the presence of miR-532-3p antagomir. [score:4]
Thus our data indicate that miR-532-3p is able to target ARC directly in DOX cardiotoxicity. [score:4]
In this study, we reveal that miR-532-3p is upregulated in cardiomyocytes administered with DOX. [score:4]
Our results suggested that enforced expression of ARC or knockdown miR-532-3p cannot completely reverse the DOX effect. [score:4]
Therefore, the development of new therapeutic strategies based on ARC, such as delivery of nucleotides that inhibit miR-532-3p, is promising for overcoming the cardiotoxicity of chemotherapy for cancer therapy. [score:4]
The expression levels of miR-532-3p were increased in DOX -treated cardiomyocytes (Figure 4b) and in mice hearts (Figure 4c) exposed to DOX. [score:3]
These data suggest that miR-532-3p targets ARC in the cascades of mitochondrial fission and apoptosis during DOX cardiotoxicity. [score:3]
When we enforced the expression of miR-532-3p in cardiomyocytes, the mitochondrial fission and death cells were significantly increased in response to the low-dose DOX (0.2  μM) treatment (Figures 5c and d). [score:3]
Overexpression of miR-532-3p sensitized low-dose DOX -induced mitochondrial fission and cell death. [score:3]
These results suggest that inhibition of miR-532-3p may be a novel strategy to conquer cardiotoxicity and not disturb chemotherapeutic effect for cancer patients. [score:3]
Overexpression of miR-532-3p had no significant effect on cell death in response to the low-dose DOX (0.2  μM) treatment (Figure 6e). [score:3]
MiR-532-3p regulates mitochondrial fission and apoptosis by targeting ARC. [score:3]
We found that overexpression of miR-532-3p had no obvious effect on ARC mRNA levels (Supplementary Figure S4e). [score:3]
Enforced expression of miR-532-3p was confirmed by qRT-PCR (Supplementary Figure S4b). [score:3]
Overexpression of miR-532-3p alone had no significant effect on mitochondrial fission and apoptosis (Figures 5a and b). [score:3]
Therefore, it seems that miR-532-3p modulates ARC expression by altering mRNA stability. [score:3]
MiR-532-3p participates in the regulation of ARC expression. [score:3]
In the present study, we have revealed for the first time that miR-532-3p -mediated suppression of ARC is a substantial causal mechanism of DOX -induced cardiac toxicity. [score:3]
Overexpression of miR-532-3p led to an obvious reduction of ARC mRNA and protein levels in cardiomyocytes (Figure 4d). [score:3]
Expression levels of miR-532-3p were not changed in Hela (Figure 7b), SGC-7901 (Figure 7c), SW-480 (Supplementary Figure S5a) and HepG-2 (Supplementary Figure S5b) cells administered with DOX. [score:3]
Knockdown miR-532-3p had no significant effect on cell death induced by DOX in these cancer cells (Figures 7d and e and Supplementary Figures S5c and d). [score:2]
Besides, we generated a mutated luciferase construct, ARC 3′UTR-Mut, and mutations were introduced into the miR-532-3p -binding site of ARC 3′UTR. [score:2]
Taken together, these results suggest that miR-532-3p regulates mitochondrial fission and apoptosis during DOX cardiotoxicity. [score:2]
MiR-532-3p sensitized cells to DOX -induced mitochondrial fission and apoptosis by targeting ARC. [score:2]
But, in cancer cells, the expression levels of miR-532-3p are low compared with cardiomyocytes and do not change in response to DOX. [score:2]
Among several miRNAs, miR-532-3p was substantially increased (Supplementary Figure S4a). [score:1]
Accordingly, we focused on miR-532-3p. [score:1]
DOX -induced apoptosis was attenuated by miR-532-3p antagomir in cardiomyocytes but not in cancer cells. [score:1]
We explored the functional role of miR-532-3p in mitochondrial fission and apoptosis in cardiomyocytes exposed to DOX. [score:1]
Our present work has identified that miR-532-3p contributes to the downregualtion of ARC. [score:1]
In addition, we measured the miR-532-3p effect on ARC expression levels in neonatal mouse cardiomyocytes isolated from ARC transgenic mice in which ARC mRNA lacks 3′UTR. [score:1]
The present study demonstrates that miR-532-3p participates in apoptosis and cardiotoxicity induced by DOX. [score:1]
However, the role of miR-532-3p in DOX -induced apoptosis in cancer cells remains largely unknown. [score:1]
We cloned ARC 3′UTR containing miR-532-3p -binding site downstream of the luciferase reporter gene (ARC 3′UTR-Wt) to examine luciferase activity driven by the 3′UTR of ARC. [score:1]
In contrast, administration of the miR-532-3p antagomir could attenuate the decrease of ARC levels in response to DOX treatment (Figure 4e). [score:1]
The potential miR-532-3p -binding site in ARC 3′UTR was shown in Figure 4a. [score:1]
It would be interesting to explore how miR-532-3p–ARC pathway is involved in this complex molecular process in the future study. [score:1]
MiR-532-3p levels were reduced by its specific antagomir (Supplementary Figure S4c). [score:1]
We explored how miR-532-3p exerts its effects on the mitochondrial network. [score:1]
The potential role of miR-532-3p in cardiomyocytes remains largely unknown. [score:1]
MiR-532-3p was expressed at low level in cancer cells, including Hela, SGC-7901, SW-480 and HepG-2, compared with cardiomyocytes (Figure 7a). [score:1]
MiR-532-3p can regulate mitochondrial fission and apoptosis in cardiomyocytes treated by DOX. [score:1]
MiR-532-3p sensitizes cardiomyocytes to apoptosis by negatively regulating ARC. [score:1]
We further investigated the effect of miR-532-3p on ARC expression in cardiomyocytes. [score:1]
As shown in Figure 4f, the wild-type 3′UTR of ARC exhibited a low luciferase activity in the presence of miR-532-3p, whereas the mutated 3′UTR did not show a significant response to miR-532-3p. [score:1]
[13] The miR-532-3p duplexes were synthesized by GenePharma Co. [score:1]
DOX -induced mitochondrial fission and apoptosis were attenuated by miR-532-3p antagomir (Figures 5e and f). [score:1]
First, we attempted to evaluate whether miR-532-3p modulated ARC expression. [score:1]
9, 46, 47, 48 It remains to be determined as to whether miR-532-3p is involved in apoptosis induced by these stimuli. [score:1]
Taken together, it seems that miR-532-3p is not involved in DOX -induced apoptotic program in cancer cells. [score:1]
We tested whether miR-532-3p is related to apoptosis in some cancer cells exposed to DOX. [score:1]
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[+] score: 23
The expressions of miR-711, miR-714, miR-744, miR-2137, miR-5130, miR-1892, miR-328, miR-346, miR-5099, and miR-705 were significantly upregulated in I/R injured heart grafts, while miR-490, miR-491, miR-210, miR-362, miR-24, miR-423, miR-128, miR-328, miR -181, and miR-532 were downregulated. [score:9]
As compared with cells under normxia, miR-711, miR-714, miR-328, miR-346, miR-210, miR-744, miR-5130, miR-181a and miR-2137 were significantly over-expressed in hypoxia/reperfusion treated cardiomyocytes, while the expression of miR-491, miR-211, miR-532, miR-185, miR-425, miR-128, miR-24 was down-regulated (Figure 4B). [score:7]
The findings of our study demonstrate that miR-711, miR-2137 miR-705, miR-5130, miR-346, miR-714, and miR-744 were significantly upregulated (>2 fold change) in I/R injured hearts, while miR-210, miR-490, miR-491, miR-425, miR-423-3p, and miR-532-3p were downregulated. [score:7]
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[+] score: 15
The resulting networks involve 48 (CTX) and 60 (MB) molecular nodes, featuring several diverse regulatory mechanisms: coexpressed miRNAs targeting the same regulated gene (e. g., miR-532-3p and miR-339-5p on Pea15 in the MB), genes encoding physically interacting or coexpressed proteins targeted by the same miRNA (e. g., miR-494-3p on both Dpysl2 and Dpysl3, and miR-140-3p on coexpressed Flot1 and Dnm1 in the CTX), and isoform-specific translational repression (e. g., Hnrnpa2b1 in the MB). [score:15]
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[+] score: 12
In contrast to clusters containing upregulated promyogenic genes, clusters with down-regulated genes in early or late myogenic differentiation were enriched for miR-335-3p, -206-3p, -322-5p, -335-5p, -351-5p, -322-3p, -133a-3p, -133b-3p, -532-5p and miR-532-3p targets (Fig 3C and S4C Table). [score:9]
Thereby, we enlarged the list of highly potential targets of miRNAs implicated in skeletal myoblast differentiation foremost miR-155, miR-206, miR-322-3p/-5p, miR-335-3p/-5p, miR-351, and miR-532-3p/-5p. [score:3]
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[+] score: 10
The TarBase dataset revealed a total of 755 putative targets for mmu-miR-532-5p, 157 for mmu-miR-690, 253 for mmu-miR696, and 11 for mmu-miR-345-3p. [score:3]
By comparison with the expression levels in total RNAs, we found 4 mitochondrial microRNAs (mmu-miR-690, mmu-miR-532-5p, mmu-miR-696, and mmu-miR-345-3p) were enriched. [score:3]
The predicted targets of miR-532-5p were Med1, NFATfatc1, and RBM20, which were reported to play crucial roles in the pathogenesis of heart failure [41– 43]. [score:3]
miR-696, miR-532, miR-690, and miR-345-3p were found to be enriched in mitochondria of failing hearts. [score:1]
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[+] score: 9
Treatment days miRNAExpression change [#] Predicted mRNA target(s)Expression change [#]GD 8/11 [†] miR-1192 ↑ Atf1, Gng4, Map3k1, Rpe, Setd2, Stxbp6, Zc3h6 ↓ miR-532-5p ↑ Atf1, Itpripl2, Stxbp6 ↓GD 14/16 [*] miR-10b ↓ Aak1 ↑ miR-184 ↓ Myl9 ↑ miR-302c ↑ Ccdc6, Mfap3, Ptpro, Rnd3, Rpl36a/r, Sema3c, Stoml3, Supt3h ↓ miR-342-5p ↓ Aak1, Cables2, Rhog ↑ miR-343 ↑ Asic4, Dcn, Gpr116, Ptpro, Stoml3 ↓ miR-449b ↓ Ina ↑PD 4/7 [†] miR-26b ↑ Adam9, Chsy1, Cnr1, Exoc8, Hs6st1, Lingo1, Map3k7, Mras, Pfkfb3, Ppm1b, Rhou, Sema6d, Shank2, Tab3, Tdrd7, Ube2j1 ↓ miR-34b-5p ↓ Kitl ↑ miR-184 ↑ Ncor2, Prkcb ↓ miR-721 ↑ Akap11, B4galt, Cnr1, Efnb2, Fam20b, Ino80, Irf1, Lrrk2, Ncoa3, Pfkfb3, Ppargc1a, Rbm9, Shank2, Spen, Sphk2, Tsc1, Wdfy3 ↓ miR-1970 ↓ Arhgap6 ↑ # Significance for expression change was 1.2-fold, p < 0.05. [score:9]
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[+] score: 7
The top 8 downregulated (hsa-miR-200c, hsa-miR-212, hsa-miR-29a, hsa-miR-532, hsa-miR-141, hsa-miR-1, hsa-miR-363, hsa-miR-187) and 8 upregulated (hsa-miR-487, hsa-miR-452, hsa-miR-1233, hsa-miR-92a, hsa-miR-106b, hsa-miR-1290, hsa-miR-320, hsa-miR-26a) miRNAs were presented in Figure 1A. [score:7]
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[+] score: 5
Interestingly, the certain miRNAs, such as miR-96, miR-140, miR-151, miR-185, miR-378, miR-455, miR-532, and miR-874, presumably targeting a 3’UTR of INSR, were upregulated by more than 1.5-fold in the liver of HFD mice compared to NFD-fed control, whereas the levels of other selected miRNAs remained unaffected (S2 Fig). [score:5]
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[+] score: 4
Thus far, only four miRNAs have been commonly reported as being upregulated in the sperm of stressed fathers, namely miR-30c, miR-204, miR-375 and miR-532. [score:4]
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[+] score: 3
Additionally, prior studies from various mo dels of retinal degeneration identified over 300 differentially expressed miRNAs 63– 90, a total of 16 common miRNAs were identified (miR-1187, miR-125b-5p, miR-331-3p, miR466d-3p, miR-467f, miR-542-3p, miR-574-5p, miR654-3p, miR669h-3p, miR-882, miR-342-3p, miR-466a-5p, miR-466d-5p, miR-706, miR-345-3p, miR532-5p). [score:3]
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[+] score: 3
Many studies have demonstrated that miRNA expression profiles are subject to change in different cells when stimulated by LPS via TLR-signaling pathways, including miR-146a, miR-155, miR-132, miR-15a/16, miR-27a and miR-532-5p [19, 20, 21, 22, 23]. [score:3]
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[+] score: 2
Other miRNAs from this paper: mmu-mir-146a, mmu-mir-34c, mmu-mir-216b
Up to now, only miR-532-3p, miR-216b, miR-34c and miR-146a were identified as potential regulators of cardiac complications of doxorubicin [17]. [score:2]
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[+] score: 1
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-21, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-33a, hsa-mir-98, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-133a-1, mmu-mir-135a-1, mmu-mir-141, mmu-mir-194-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-203a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-200b, mmu-mir-300, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-141, hsa-mir-194-1, 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-21a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-343, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, mmu-mir-200c, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, mmu-mir-29b-2, mmu-mir-135a-2, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-326, hsa-mir-135b, mmu-mir-133a-2, 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-21, rno-mir-26b, rno-mir-27b, rno-mir-27a, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-33, rno-mir-98, rno-mir-126a, rno-mir-133a, rno-mir-135a, rno-mir-141, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-203a, rno-mir-211, rno-mir-218a-2, rno-mir-218a-1, rno-mir-300, hsa-mir-429, mmu-mir-429, rno-mir-429, hsa-mir-485, hsa-mir-511, hsa-mir-532, rno-mir-133b, mmu-mir-485, rno-mir-485, hsa-mir-33b, mmu-mir-702, mmu-mir-343, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, hsa-mir-300, mmu-mir-511, rno-mir-466b-1, rno-mir-466b-2, rno-mir-532, rno-mir-511, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466b-8, hsa-mir-3120, rno-mir-203b, rno-mir-3557, rno-mir-218b, rno-mir-3569, rno-mir-133c, rno-mir-702, rno-mir-3120, hsa-mir-203b, mmu-mir-344i, rno-mir-344i, rno-mir-6316, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-3569, rno-let-7g, rno-mir-29c-2, rno-mir-29b-3, rno-mir-466b-3, rno-mir-466b-4, mmu-mir-203b
Type of site Context+ Context Structure Energy Is experimental validated rno-miR-326-5p MIMAT0017028 3 8mer 7mer-m8 imperfect −0.442 −0.242 431 −65.97 TRUE rno-miR-485-5p MIMAT0003203 2 7mer-m8 −0.343 −0.372 290 −34.96 TRUE rno-miR-300-5p MIMAT0004743 1 8mer −0.338 −0.421 156 −15.16 TRUE rno-miR-702-5p MIMAT0017884 1 8mer −0.317 −0.274 142 −13.86 TRUE rno-miR-203b-3p MIMAT0017800 2 7mer-m8 −0.298 −0.421 295 −29.93 TRUE rno-miR-33-3p MIMAT0017104 2 8mer 7mer-m8 −0.297 −0.813 305 −22.7 TRUE rno-miR-466b-3p MIMAT0017285 1 8mer −0.295 −0.47 159 −15.26 TRUE rno-miR-532-5p MIMAT0005322 1 7mer-m8 −0.268 −0.302 151 −10.71 TRUE rno-miR-511-5p MIMAT0012829 1 7mer-m8 −0.268 −0.302 152 −10.37 TRUE rno-miR-343 MIMAT0000591 1 7mer-m8 −0.262 −0.24 140 −13.75 TRUE rno-miR-203a-3p MIMAT0000876 1 8mer −0.245 −0. [score:1]
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