Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/98227
Full metadata record
DC FieldValueLanguage
dc.contributor.authorZhang, Chenen
dc.contributor.authorTan, Chek Kunen
dc.contributor.authorMcFarlane, Craigen
dc.contributor.authorSharma, Mridulaen
dc.contributor.authorTan, Nguan Soonen
dc.contributor.authorKambadur, Ravien
dc.date.accessioned2013-07-29T04:18:43Zen
dc.date.accessioned2019-12-06T19:52:16Z-
dc.date.available2013-07-29T04:18:43Zen
dc.date.available2019-12-06T19:52:16Z-
dc.date.copyright2012en
dc.date.issued2012en
dc.identifier.citationZhang, C., Tan, C. K., McFarlane, C., Sharma, M., Tan, N. S., & Kambadur, R. (2012). Myostatin-null mice exhibit delayed skin wound healing through the blockade of transforming growth factor- β signaling by decorin. American Journal of Physiology: Cell Physiology, 302(8), C1213-C1225.en
dc.identifier.urihttps://hdl.handle.net/10356/98227-
dc.description.abstractMyostatin (Mstn) is a secreted growth and differentiation factor that belongs to the transforming growth factor-β (TGF-β) superfamily. Mstn has been well characterized as a regulator of myogenesis and has been shown to play a critical role in postnatal muscle regeneration. Herein, we report for the first time that Mstn is expressed in both epidermis and dermis of murine and human skin and that Mstn-null mice exhibited delayed skin wound healing attributable to a combination of effects resulting from delayed epidermal reepithelialization and dermal contraction. In epidermis, reduced keratinocyte migration and protracted keratinocyte proliferation were observed, which subsequently led to delayed recovery of epidermal thickness and slower reepithelialization. Furthermore, primary keratinocytes derived from Mstn-null mice displayed reduced migration capacity and increased proliferation rate as assessed through in vitro migration and adhesion assays, as well as bromodeoxyuridine incorporation and Western blot analysis. Moreover, in dermis, both fibroblast-to-myofibroblast transformation and collagen deposition were concomitantly reduced, resulting in a delayed dermal wound contraction. These decreases are due to the inhibition of TGF-β signaling. In agreement, the expression of decorin, a naturally occurring TGF-β suppressor, was elevated in Mstn-null mice; moreover, topical treatment with TGF-β1 protein rescued the impaired skin wound healing observed in Mstn-null mice. These observations highlight the interplay between TGF-β and Mstn signaling pathways, specifically through Mstn regulation of decorin levels during the skin wound healing process. Thus we propose that Mstn agonists might be beneficial for skin wound repair.en
dc.language.isoenen
dc.relation.ispartofseriesAmerican journal of physiologyen
dc.rights© 2012 the American Physiological Society.en
dc.subjectDRNTU::Science::Biological sciencesen
dc.titleMyostatin-null mice exhibit delayed skin wound healing through the blockade of transforming growth factor- β signaling by decorinen
dc.typeJournal Articleen
dc.contributor.schoolSchool of Biological Sciencesen
dc.identifier.doi10.1152/ajpcell.00179.2011en
item.fulltextNo Fulltext-
item.grantfulltextnone-
Appears in Collections:SBS Journal Articles

Google ScholarTM

Check

Altmetric


Plumx

Items in DR-NTU are protected by copyright, with all rights reserved, unless otherwise indicated.