Identification of microRNAs involved in dexamethasone-induced muscle atrophy

Shen, He; Teng, Liu; Fu, Liangliang; Song, Zhao; Fan, Bin; Cao, Jianhua; Li, Xinyun

doi:10.1007/s11010-013-1692-9

Cited by 43 publications

(38 citation statements)

References 46 publications

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“…Recent evidence suggests that miRNAs are involved in modulation of atrophy, proliferation and differentiation of skeletal muscles (20,24,25). A previous study observed that miR-351 is transiently increased in early days of muscle regeneration (26).…”

Section: Discussionmentioning

confidence: 99%

“…However, the involvement of miRNAs in muscle-associated biological processes has not been fully investigated. To our knowledge, it has only been reported that miR-1 and miR-133 are able to promote differentiation and proliferation of the skeletal and cardiac muscle cells (19), and the expression of miR-351 in differentiated C2C12 cells is upregulated following treatment with dexamethasone (20). The underlying mechanisms, however, are still to be further explored.…”

Section: Introductionmentioning

confidence: 92%

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MicroRNA-351 inhibits denervation-induced muscle atrophy by targeting TRAF6

Qiu

Dai

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. MicroRNAs (miRs) have been observed to be involved in the modulation of various physiopathological processes. However, the impacts of miRNAs on muscle atrophy have not been fully investigated. In the present study, the results demonstrated that miR-351 was differentially expressed in the tibialis anterior (TA) muscle at various times following sciatic nerve transection, and the time-dependent expression profile of miR-351 was inversely correlated with that of tumor necrosis factor receptor-associated factor 6 (TRAF6) at the mRNA and protein levels. The dual luciferase reporter assay indicated that miR-351 was able to significantly downregulate the expression levels of TRAF6 by directly targeting the 3'-untranslated region of TRAF6. Overexpression of miR-351 inhibited a significant decrease in the wet weight ratio or cross-sectional area of the TA muscle following sciatic nerve transection. Western blot analysis indicated that the protein expression levels of TRAF6, muscle ring-finger protein 1 (MuRF1) and muscle atrophy F-box (MAFBx) in denervated TA muscles were suppressed by overexpression of miR-351. These results demonstrate that miR-351 inhibits denervation-induced atrophy of TA muscles following sciatic nerve transection at least partially through negative regulation of TRAF6 as well as MuRF1 and MAFBx, the two downstream signaling molecules of TRAF6.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 92%

MicroRNA-351 inhibits denervation-induced muscle atrophy by targeting TRAF6

Qiu

Dai

et al. 2016

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

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“…This suggests that the endogenous levels of miR-181 are normally sufficient to reach effect-exerting plateau [116]. Other regulators of the balance between proliferation and differentiation in myogenic cells are miR-322 and miR-503, which target cell cycle promoter Cdc-25a, although the evidence is at present limited to one myoblast cell line in vitro [117,118]. As in cardiac myogenesis, epigenetic and post-transcriptional controls are complexly entwined with miRs in skeletal muscle formation [119].…”

Section: Skeletal Myogenesis and Mirsmentioning

confidence: 99%

The mesmiRizing complexity of microRNAs for striated muscle tissue engineering

Quattrocelli

Sampaolesi

2015

Advanced Drug Delivery Reviews

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microRNAs (miRs) are small non-protein-coding RNAs, able to post-transcriptionally regulate many genes and exert pleiotropic effects. Alteration of miR levels in tissues and in the circulation has been associated with various pathological and regenerative conditions. In this regard, tissue engineering of cardiac and skeletal muscles is a fascinating context for harnessing the complexity of miR-based circuitries and signals. In this review, we will focus on miR-driven regulation of cardiac and skeletal myogenic routes in homeostatic and challenging states. Furthermore, we will survey the intriguing perspective of exosomal and circulating miRs as novel paracrine players, potentially useful for current and future approaches of regenerative medicine for the striated muscles.

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“…Growing evidence has suggested that miRNAs participate in a series of biological processes such as cell proliferation, apoptosis, immune response, as well as many diseases 12,13) .…”

Section: Introductionmentioning

confidence: 99%

Identification of the Differentially Expressed microRNAs Involved in Cleft Palate Induced by Retinoic Acid (RA) in Mouse Model

Wei

Huang

et al. 2018

J. Hard Tissue Biology.

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Identifying the diff erentially expressed miRNAs in cleft palate, in order to study the molecular mechanism in the development and progress of cleft palate. C57BL/6J mice were used to establish the RA induced cleft palate mouse model. Nine pairs of tissues were obtained on embryonic day 15.5 (E15.5). Total RNA was extracted and miRNAs microarray chip was used to screen the miRNAs. Real-time quantitative PCR (RT-qPCR) was used to verify the miRNAs microarray chip results. Cleft palate related genes targeted by the miRNAs were predicted by TargetScan and miRTarBase, and functional annotation clustering of Gene Ontology (GO) term and KEGG signaling pathways in DAVID were used to analysis these target genes. 1265 miRNAs were identifi ed in cleft palate, and among them 31 were diff erentially expressed (p < 0.01, fold change > 1.5), including 17 up-regulated and 14 down-regulated miRNAs in cleft palate. 7 up-regulated miRNAs (mmu-miR181a-5p, mmu-miR-410-3p, mmu-miR-3960, mmu-miR-1224-5p, mmu-miR-3970, mmu-let-7e-5p and mmu-miR-1907) and 3 down-regulated miRNAs (mmu-miR-140-3p, mmu-miR-351-5p and mmu-miR-503-5p) were validated by RT-qPCR, and mmumiR-181a-5p and mmu-miR-410-3p were in concordance with those of miRNAs microarray chip detection. 484 target genes were predicted and proven by TargetScan and miRTarBase. GO term showed that RA-induced cleft palate was associated with enrichments in miRNAs involved in embryo development, osteoblast diff erentiation and so on. KEGG signaling pathways analysis indicated that the diff erentially expressed miRNAs were involved in MAPK, TGFβ and WNT signaling pathways. 10 diff erentially expressed miRNAs in cleft palate have been identifi ed. These miRNAs and their target genes may become new therapeutic targets for cleft palate.

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Identification of microRNAs involved in dexamethasone-induced muscle atrophy

Cited by 43 publications

References 46 publications

MicroRNA-351 inhibits denervation-induced muscle atrophy by targeting TRAF6

MicroRNA-351 inhibits denervation-induced muscle atrophy by targeting TRAF6

The mesmiRizing complexity of microRNAs for striated muscle tissue engineering

Identification of the Differentially Expressed microRNAs Involved in Cleft Palate Induced by Retinoic Acid (RA) in Mouse Model

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