Necl2 Regulates Epidermal Adhesion And Wound Repair

The study explored the role of Necl2 in epidermal adhesion and wound repair, finding it crucial for maintaining epidermal integrity and efficient wound healing. Necl2 was highly expressed in bulge stem cells of hair follicles and influenced keratinocyte adhesion and motility. Overexpression increased intercellular adhesion and reduced motility, delaying wound healing, but did not affect normal epidermal homeostasis. Necl2-null and transgenic mice showed normal epidermis, but wound healing was delayed in Necl2-overexpressing mice, linked to reduced proliferation and increased CASK and E-cadherin at wound edges. The study suggested Necl2's role in stabilizing cell-cell adhesion and regulating stem cell quiescence, impacting wound repair processes.