Abstract
BackgroundMatricellular proteins, including periostin, are important for tissue regeneration.Methods and FindingsPresently we investigated the function of periostin in cutaneous wound healing by using periostin-deficient (−/−) mice. Periostin mRNA was expressed in both the epidermis and hair follicles, and periostin protein was located at the basement membrane in the hair follicles together with fibronectin and laminin γ2. Periostin was associated with laminin γ2, and this association enhanced the proteolytic cleavage of the laminin γ2 long form to produce its short form. To address the role of periostin in wound healing, we employed a wound healing model using WT and periostin−/− mice and the scratch wound assay in vitro. We found that the wound closure was delayed in the periostin−/− mice coupled with a delay in re-epithelialization and with reduced proliferation of keratinocytes. Furthermore, keratinocyte proliferation was enhanced in periostin-overexpressing HaCaT cells along with up-regulation of phosphorylated NF-κB.ConclusionThese results indicate that periostin was essential for keratinocyte proliferation for re-epithelialization during cutaneous wound healing.
Highlights
Wound healing, the tissue repair process, is accomplished through the following 3 stages: inflammation, proliferation, and remodeling [1]
These results indicate that periostin was essential for keratinocyte proliferation for re-epithelialization during cutaneous wound healing
Expression of periostin mRNA and protein in normal mouse and human skin Firstly, we examined the periostin mRNA expression in normal mouse skin by performing mRNA in situ hybridization, and found that periostin mRNA was expressed in the bulge region of the hair follicle, especially in the outer cells along the basement membrane (Fig 1Aa, arrow) not in the inner cells (Fig. 1Aa, arrowhead), and its protein was localized at the basement membrane of the follicular bulge region (Fig. 1Ab, brown stain)
Summary
The tissue repair process, is accomplished through the following 3 stages: inflammation, proliferation, and remodeling [1]. Keratinocytes function for epidermis maturation and wound contraction; and the fibroblasts differentiate into a smooth muscle actin (aSMA)-positive myofibroblasts [2]. These latter cells express various extracellular matrix (ECM) proteins such as collagens and fibronectin for remodeling the granulation tissue into normal tissue [3]. Keratinocyte proliferation and migration are early events in wound re-epithelialization. Keratinocytes initially respond to an epidermal defect by proliferating and migrating from the free edges of the wound.
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