Journal
JOURNAL OF CELL SCIENCE
Volume 125, Issue 1, Pages 121-132Publisher
COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.087841
Keywords
alpha-Smooth muscle actin; Contraction; Matricellular protein; Myofibroblast; Periostin; Wound healing
Categories
Funding
- Canadian Foundation for Innovation [18742]
- Canadian Institutes of Health Research Institute of Musculoskeletal Health and Arthritis [IMH-94010]
- National Sciences and Engineering Research Council of Canada
- Arthritis Research UK
- Riley Children's Foundation
- Indiana University Department of Pediatrics (Neonatal-Perinatal Medicine]
- National Institute of Health [HL092508]
- Division Of Materials Research
- Direct For Mathematical & Physical Scien [1006734] Funding Source: National Science Foundation
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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 alpha-smooth muscle actin (alpha-SMA) within the granulation tissue. Delivery of recombinant human periostin by electrospun collagen scaffolds restored alpha-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-beta 1-integrin and to the FAK and Src inhibitor PP2. We propose that periostin promotes wound contraction by facilitating myofibroblast differentiation and contraction.
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