Role of periostin in skin wound healing and pathologic scar formation

Abstract

[1,6,9] Elliott et al[6] reported that full-thickness skin wounds were significantly larger in periostin-knockout mice than those in wild type mice at 5 and 7 days after wounding, and α-smooth muscle actin (α-SMA) was significantly down-regulated in wounds of periostin-deficient-mice. [...]Ontsuka et al[7] reported that the intervals for wound closure were significantly extended in periostin-knockout mice than those in wild type mice, suggesting that periostin could affect wound re-epithelialization. Compared to those untreated mice, addition of periostin- and CCN2-containing scaffolds suppresses neutrophil persistence, and increases the closure rate, mesenchymal cell infiltration, collagen density, and revascularization of wounds. Besides promoting wound healing itself, periostin also reportedly enhances the function of adipose-derived stem cells (ADSCs) in promoting wound healing. Since spatiotemporal expression of periostin is reportedly important to promote wound healing,[4] the results from Nunomura's study remind us that it is potentially infeasible to promote skin wound healing by simply up-regulating periostin, unlike regulated spatiotemporal expression of periostin, constitutive transgenic periostin expression may in turn interrupt normal wound closure. Periostin reportedly affects pathologic scar formation by regulating the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) and ERK pathway and ras homolog gene family member A/Rho-associated protein kinase (RhoA/ROCK) pathway, which are necessary for the proliferation, differentiation, migration, invasion, and matrix collagen synthesis of pathologic scar fibroblasts.