Necl2 Regulates Epidermal Adhesion And Wound Repair

The study demonstrated that the intercellular adhesion protein Necl2 was highly expressed in bulge stem cells of human and mouse hair follicles and played a role in regulating epidermal stem cell quiescence and location. Overexpression of Necl2 in human keratinocytes increased calcium-independent intercellular adhesion, inhibited cell motility, and delayed in vitro wound healing, without affecting terminal differentiation. In vivo, Necl2-null and transgenic mice showed normal epidermal homeostasis, but Necl2 overexpression led to delayed wound healing, reduced proliferation, and increased CASK and E-cadherin levels at wound edges. These findings suggested that Necl2 influenced stem cell behavior and wound repair processes.