ESC Biomarkers and their role in wound healing
Wound healing involves a complex orchestration of processes that suppress infection and restore the dermal barrier. Healing begins immediately following the laceration to the epidermis with hemostasis, which includes initial vasoconstriction and thrombocyte clumping. Following is an influx of fibroblasts (which help clot the wound opening), and inflammatory macrophages. Next, granulation tissue creates a framework for forming permanent connective tissue. This last stage involves of matrix fiber reconstruction, angiogenesis, and cell differentiation and proliferation, and epidermal remodeling [1]. The previously mentioned biomarkers are mainly involved in this last stage of the wound healing process.
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The cytoplasmic portion is connected to the biomarker β-catenin coupled to an α-catenin molecule that is directly attached to an intracellular actin filament [2]. Cadherin-catenin-actin complexes ensure mechanical adhesion of epithelial cells. During wound repair, E-cadherin (epithelial cadherin) alters cell adhesion to prepare for keratinocyte migration. Previous studies show that E-cadherin is downregulated in basal epithelial cells surrounding the insult area during reepithelialization [3]. It was found that when E-cadherin is not downregulated (by knocking out the epidermal regulatory gene Ctip2), epithelial cells are more tightly packed together, thus inhibiting keratinocyte migration, and consequentially reepithelialization itself [3]. Similarly, a recent study by Keswell, D et al, shows that E-cadherin expression promotes melanocyte migration into the wound area, as well as decreased keratinocyte attachment