| Title: | Transgenic Overexpression of miR-133a in Skeletal Muscle |
| Author: |
Deng, Zhongliang; Chen, Jian-Fu; Wang, Da-Zhi
Note: Order does not necessarily reflect citation order of authors. |
| Citation: | Deng, Zhongliang, Jian-Fu Chen, and Da-Zhi Wang. 2011. Transgenic overexpression of miR-133a in skeletal muscle. BMC Musculoskeletal Disorders 12:115. |
| Full Text & Related Files: |
3125252.pdf (2.548Mb; PDF)
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| Abstract: | Background: MicroRNAs (miRNAs) are a class of non-coding regulatory RNAs of ~22 nucleotides in length. miRNAs regulate gene expression post-transcriptionally, primarily by associating with the 3' untranslated region (UTR) of their regulatory target mRNAs. Recent work has begun to reveal roles for miRNAs in a wide range of biological processes, including cell proliferation, differentiation and apoptosis. Many miRNAs are expressed in cardiac and skeletal muscle, and dysregulated miRNA expression has been correlated with muscle-related disorders. We have previously reported that the expression of muscle-specific miR-1 and miR-133 is induced during skeletal muscle differentiation and miR-1 and miR-133 play central regulatory roles in myoblast proliferation and differentiation in vitro. Methods: In this study, we measured the expression of miRNAs in the skeletal muscle of mdx mice, an animal model for human muscular dystrophy. We also generated transgenic mice to overexpress miR-133a in skeletal muscle. Results: We examined the expression of miRNAs in the skeletal muscle of mdx mice. We found that the expression of muscle miRNAs, including miR-1a, miR-133a and miR-206, was up-regulated in the skeletal muscle of mdx mice. In order to further investigate the function of miR-133a in skeletal muscle in vivo, we have created several independent transgenic founder lines. Surprisingly, skeletal muscle development and function appear to be unaffected in miR-133a transgenic mice. Conclusions: Our results indicate that miR-133a is dispensable for the normal development and function of skeletal muscle. |
| Published Version: | doi:10.1186/1471-2474-12-115 |
| Other Sources: | http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3125252/pdf/ |
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| Citable link to this page: | http://nrs.harvard.edu/urn-3:HUL.InstRepos:5978754 |
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