Periostin modulates myofibroblast differentiation during full-thickness cutaneous wound repair

Elliott, C.G., Wang, J., Guo, X., Xu, S.W., Eastwood, M., Guan, J., Leask, A., Conway, S.J., Hamilton, D.W. and Shi-Wen, X. 2012. Periostin modulates myofibroblast differentiation during full-thickness cutaneous wound repair. Journal of Cell Science. 125 (1), pp. 121-132.

TitlePeriostin modulates myofibroblast differentiation during full-thickness cutaneous wound repair
AuthorsElliott, C.G., Wang, J., Guo, X., Xu, S.W., Eastwood, M., Guan, J., Leask, A., Conway, S.J., Hamilton, D.W. and Shi-Wen, X.
Abstract

The matricellular protein periostin is expressed in the skin. Although periostin has been hypothesized to contribute to dermal homeostasis and repair, this has not been directly tested. To assess the contribution of periostin to dermal healing, 6 mm full-thickness excisional wounds were created in the skin of periostin-knockout and wild-type, sex-matched control mice. In wild-type mice, periostin was potently induced 5–7 days after wounding. In the absence of periostin, day 7 wounds showed a significant reduction in myofibroblasts, as visualized by expression of α-smooth muscle actin (α-SMA) within the granulation tissue. Delivery of recombinant human periostin by electrospun collagen scaffolds restored α-SMA expression. Isolated wild-type and knockout dermal fibroblasts did not differ in in vitro assays of adhesion or migration; however, in 3D culture, periostin-knockout fibroblasts showed a significantly reduced ability to contract a collagen matrix, and adopted a dendritic phenotype. Recombinant periostin restored the defects in cell morphology and matrix contraction displayed by periostin-deficient fibroblasts in a manner that was sensitive to a neutralizing anti-β1-integrin and to the FAK and Src inhibitor PP2. We propose that periostin promotes wound contraction by facilitating myofibroblast differentiation and contraction.

JournalJournal of Cell Science
Journal citation125 (1), pp. 121-132
ISSN0021-9533
YearJan 2012
PublisherThe Company of Biologists Ltd.
Digital Object Identifier (DOI)doi:10.1242/jcs.087841
Publication dates
PublishedJan 2012

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