Vitamin D(3) signalling to mast cells: A new regulatory axis

Int J Biochem Cell Biol. 2011 Jan;43(1):41-6. doi: 10.1016/j.biocel.2010.10.011. Epub 2010 Oct 23.

Abstract

Excessive sun exposure or high acute doses of ultraviolet (UV)-B radiation promote cutaneous inflammation and genetic mutations, both of which can ultimately contribute to skin carcinogenesis. A major mediator synthesized in the epidermis in response to UVB irradiation is the secosteroid hormone vitamin D(3), and as such, considerable attention is now turning to the many physiologic processes that it regulates. Recent studies have uncovered an immunoregulatory interaction between vitamin D(3) and dermal mast cells for optimal protection against pathogenic outcomes associated with chronic UVB irradiation of the skin. Most biological effects of vitamin D(3), such as the regulation of transcription in target genes, occur when it binds to its nuclear receptor; however, some actions can also occur via a non-genomic signalling pathway. This review will focus on the relative importance of both pathways in the regulation of vitamin D(3)-mediated UVB protection and will highlight exciting recent findings that point to new research directions.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cholecalciferol* / metabolism
  • Cholecalciferol* / pharmacology
  • Cytokines / metabolism
  • Gene Expression Regulation / immunology
  • Gene Expression Regulation / physiology*
  • Humans
  • Immunomodulation
  • Mast Cells / metabolism
  • Mast Cells / pathology
  • Mast Cells / physiology
  • Mice
  • Receptors, Calcitriol / immunology
  • Receptors, Calcitriol / metabolism
  • Signal Transduction* / immunology
  • Signal Transduction* / physiology
  • Skin / drug effects
  • Skin / metabolism
  • Skin / pathology
  • Skin Neoplasms / metabolism
  • Skin Neoplasms / pathology
  • Ultraviolet Rays / adverse effects

Substances

  • Cytokines
  • Receptors, Calcitriol
  • Cholecalciferol