Published online Jul 26, 2020. doi: 10.4252/wjsc.v12.i7.604
Peer-review started: February 25, 2020
First decision: April 22, 2020
Revised: May 18, 2020
Accepted: June 10, 2020
Article in press: June 10, 2020
Published online: July 26, 2020
Processing time: 151 Days and 8.7 Hours
Epidermal stem cells (SCs) residing in the skin play an essential role for epidermal regeneration during cutaneous wound healing. Upon injury, distinct epidermal SCs residing in the interfollicular epidermis and/or hair follicles are activated to proliferate. Subsequently, SCs and progeny migrate, differentiate and restore the epidermis. We review a role of the vitamin D signaling through its receptor of vitamin D receptor (Vdr) in these processes. Vdr conditional knockout (cKO) mouse skin experiences a delay in wound re-epithelialization under low dietary calcium conditions, stimulating our efforts to examine a cooperative role of Vdr with calcium signaling through the calcium sensing receptor in the epidermis. We review the role of vitamin D and calcium signaling in different processes essential for injury induced epidermal regeneration during cutaneous wound repair. First, we discuss their roles in self-renewal of epidermal SCs through β-catenin signaling. Then, we describe epidermal remodeling, in which SCs and progeny migrate and differentiate to restore the epidermis, events controlled by the E-cadherin mediated adherens junction signaling. Finally, we discuss the potential mechanisms for vitamin D and calcium signaling to regulate injury induced epidermal regeneration mutually and interdependently.
Core tip: Vitamin D and calcium signaling play critical roles in epidermal stem cells and progeny to regenerate the epidermis during cutaneous wound healing. Their regulation of these processes is mediated at least in part through β-catenin and E-cadherin mediated adherens junction signaling.