Pannexin-3 deficiency delays skin wound healing in mice due to defects in channel functionality

Pannexin-3 (Panx3) is a gap junction protein and is required for regulating cell cycle exit and the differentiation of osteoblasts and chondrocytes during skeletal development. However, the role of Panx3 in skin tissue regeneration remains unclear. Following dorsal skin punch biopsies, Panx3 knockout mice exhibited a significant delay in wound healing with insufficient re-epithelialization, decreased inflammatory reaction and reduced collagen remodeling. Panx3 expression coincided with inflammatory reactions both in vivo and in vitro.