Role of vitamin D and calcium signaling in epidermal wound healing

Abstract

Purpose This review will discuss the role of vitamin D and calcium signaling in the epidermal wound response with particular focus on the stem cells of the epidermis and hair follicle that contribute to the wounding response. Methods Selected publications relevant to the mechanisms of wound healing in general and the roles of calcium and vitamin D in wound healing in particular were reviewed. Results Following wounding the stem cells of the hair follicle and interfollicular epidermis are activated to proliferate and migrate to the wound where they take on an epidermal fate to re-epithelialize the wound and regenerate the epidermis. The vitamin D and calcium sensing receptors (VDR and CaSR, respectively) are expressed in the stem cells of the hair follicle and epidermis where they play a critical role in enabling the stem cells to respond to wounding. Deletion of Vdr and/or Casr from these cells delays wound healing. The VDR is regulated by co-regulators such as the Med 1 complex and other transcription factors such as Ctnnb (beta-catenin) and p63. The formation of the Cdh1/Ctnn (E-cadherin/catenin) complex jointly stimulated by vitamin D and calcium plays a critical role in the activation, migration, and re-epithelialization processes. Conclusion Vitamin D and calcium signaling are critical for the ability of epidermal and hair follicle stem cells to respond to wounding. Vitamin D deficiency with the accompanying decrease in calcium signaling can result in delayed and/or chronic wounds, a major cause of morbidity, loss of productivity, and medical expense.

Lactobacillus johnsonii LJO02 (DSM 33828) Cell-Free Supernatant and Vitamin D Improve Wound Healing and Reduce Interleukin-6 Production in Staphylococcus aureus-Infected Human Keratinocytes

“…Considering that vitamin D 100 nM is equivalent to 38.4 ng/mL, this concentration is within the physiological range [ 33 ]. According to Bikle et al, the physiological concentration of vitamin D promotes in vitro wound healing, whereas vitamin D deficiency results in delayed scratch re-epithelialization or chronic wounds, suggesting the usefulness of vitamin D supplementation only in a deficiency context [ 34 ].…”

N,N-Dimethylglycine Sodium Salt Exerts Marked Anti-Inflammatory Effects in Various Dermatitis Models and Activates Human Epidermal Keratinocytes by Increasing Proliferation, Migration, and Growth Factor Release

“…Elevation of the intracellular Ca 2+ concentration is one of the key intracellular signaling pathways that regulate practically all keratinocytes' functions, including, but not limited to, proliferation, differentiation, migration, wound healing, growth factor release, inflammatory and immune signaling pathways, etc. [80][81][82][83][84][85][86]. Therefore-albeit further experiments are needed to uncover how the intracellular Ca 2+ concentration elevated by DMG-Na is mechanistically linked to such signaling systems as, e.g., certain inflammatory signal transduction pathways (NF-κB, MAPK, or JAK-STAT) or the release of VEGF and other mediators-it is highly possible that the quite versatile effects (stimulation of proliferation, migration, and growth factor release; anti-inflammatory and antioxidant action) of DMG-Na are mediated (or at least closely linked) to its action on elevating the intracellular level of the 'universal' signal transducer Ca 2+ .…”

Osteoporosis and dermatoporosis: a review on the role of vitamin D

“…Impaired wound healing is a common characteristic of dermatoporotic skin ( 2 ). VD has been demonstrated to improve wound healing by encouraging cell proliferation and migration and facilitating collagen synthesis ( 133 ). By supporting the healing process, VD may help improve the recovery time of wounds and minimize the risk of complications in dermatoporotic skin.…”