Please use this identifier to cite or link to this item: https://doi.org/10.1242/jcs.136648
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dc.titleSharp-1 regulates TGF-β signaling and skeletal muscle regeneration
dc.contributor.authorAcharjee, S.
dc.contributor.authorChung, T.-K.
dc.contributor.authorGopinadhan, S.
dc.contributor.authorShankar, S.R.
dc.contributor.authorWang, Y.
dc.contributor.authorLi, L.
dc.contributor.authorVercherat, C.
dc.contributor.authorGulbagci, N.T.
dc.contributor.authorRossner, M.
dc.contributor.authorTaneja, R.
dc.date.accessioned2016-07-08T09:30:02Z
dc.date.available2016-07-08T09:30:02Z
dc.date.issued2014-02-01
dc.identifier.citationAcharjee, S., Chung, T.-K., Gopinadhan, S., Shankar, S.R., Wang, Y., Li, L., Vercherat, C., Gulbagci, N.T., Rossner, M., Taneja, R. (2014-02-01). Sharp-1 regulates TGF-β signaling and skeletal muscle regeneration. Journal of Cell Science 127 (3) : 599-608. ScholarBank@NUS Repository. https://doi.org/10.1242/jcs.136648
dc.identifier.issn00219533
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/125671
dc.description.abstractSharp-1 is a basic helix-loop-helix (bHLH) transcriptional repressor that is involved in a number of cellular processes. Our previous studies have demonstrated that Sharp-1 is a negative regulator of skeletal myogenesis and it blocks differentiation of muscle precursor cells by modulating the activity of MyoD. In order to understand its role in pre-and post-natal myogenesis, we assessed skeletal muscle development and freeze-injury-induced regeneration in Sharp-1-deficient mice. We show that embryonic skeletal muscle development is not impaired in the absence of Sharp-1; however, post-natally, the regenerative capacity is compromised. Although the initial phases of injury-induced regeneration proceed normally in Sharp-1-/- mice, during late stages, the mutant muscle exhibits necrotic fibers, calcium deposits and fibrosis. TGF-β expression, as well as levels of phosphorylated Smad2 and Smad3, are sustained in the mutant tissue and treatment with decorin, which blocks TGF-β signaling, improves the histopathology of Sharp-1-/- injured muscles. In vitro, Sharp-1 associates with Smad3, and its overexpression inhibits TGF-β-and Smad3-mediated expression of extracellular matrix genes in myofibroblasts. These results demonstrate that Sharp-1 regulates muscle regenerative capacity, at least in part, by modulation of TGF-β signaling. © 2014. Published by The Company of Biologists Ltd.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1242/jcs.136648
dc.publisherCompany of Biologists
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceScopus
dc.subjectDegeneration
dc.subjectFibrosis
dc.subjectMyofibroblast
dc.subjectRegeneration
dc.subjectSkeletal muscle
dc.subjectTGF-β
dc.typeArticle
dc.contributor.departmentDEPT OF PHYSIOLOGY
dc.description.doi10.1242/jcs.136648
dc.description.sourcetitleJournal of Cell Science
dc.description.volume127
dc.description.issue3
dc.description.page599-608
dc.description.codenJNCSA
dc.identifier.isiut000331201600011
dc.published.statePublished
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