Figure 6.

A proposed model in which Vdr and calcium signaling concurrently control wound re-epithelialization through regulation of AJ formation and β-catenin signaling. (a) Summary showing deficiency in both Vdr and Casr prevents proliferation and migration of keratinocytes to delay wound (lightning bolt) re-epithelialization of epidermis. (b) A proposed action of vitamin D and calcium signaling, in which they cross-talk to regulate AJ formation, β-catenin signaling through AJ signaling, and desmosome function through calcium-regulated PKCα activity. Both Vdr and Casr concurrently control β-catenin signaling and AJ signaling, which govern adhesion, migration, and differentiation of regenerating keratinocytes at the wound edge.