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Cell Journal، جلد ۱۶، شماره Suppl ۱، صفحات ۸۹-۸۹
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عنوان انگلیسی Ps-57: MiR-214 and MiR-135 Have Conflicting Expression Pattern during C2C12 Myoblast to Myocyte Differentiation
چکیده انگلیسی مقاله Objective: The process of generating muscle is highly complex and requires a broad spectrum of signaling molecules. MicroRNAs are evolutionarily conserved small RNAs that post-transcriptionally regulate gene expression and have emerged as critical regulators of skeletal muscle development. Materials and Methods: In this study, mouse myoblast cells (C2C12) differentiation upon partial serum deprivation from myoblast cells into myocytes is confirmed by positive Immunocytochemistry for specific skeletal marker, myosin. Using Target Scan 6.2, miRwalk and RNAhybrid, we found that miR-214 and miR- 135 targeted several signal molecules, which are regulator of myogenesis process and insulin pathway as such insulin receptor substrate 2 (IRS 2) and insulin receptor (INSR). Results: After qRT-PCR analysis, we recognized miR-135 as a novel miRNA involved in skeletal muscle development which had different expression level during myogenic differentiation. According to our data, miR-135 was up-regulated but miR-214 expression was down-regulated in myocytes. Interestingly, it was shown that the expression level of IRS-2 and INSR, were up-regulated in differentiated cells in comparison with undifferentiated one. Conclusion: Using a bioinformatics approach, we identified IRS-2 and INSR, as targets of miR-214. Decreased expression of miR-214 in myocytes in comparision with myoblasts was accompanied with overexpression of IRS-2 and INSR, leading to myogenic differentiation progression. According to previous studies, it has been reported that muscle differentiation is blocked by decreased IRS1/2 and PI3k activity. Interestingly our study demonstrated that down-regulation of miR-214 may accelerate myogenesis because of increasing its target mRNA, IRS-2 during myogenic differentiation. In summary, our data identifies miR- 214 and miR-135 as potential regulator of myogenesis through regulation of IRS/PI3K pathway.
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نشانی اینترنتی http://celljournal.org/journal/article/abstract/383
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