1Alpha,25-dihydroxyvitamin D3 protects human keratinocytes from apoptosis by the formation of sphingosine-1-phosphate

J Invest Dermatol. 2001 Nov;117(5):1241-9. doi: 10.1046/j.0022-202x.2001.01496.x.

Abstract

Owing to its ability to induce growth arrest and differentiation of keratinocytes, 1alpha,25-dihydroxyvitamin D3 and its analogs are useful for the treatment of hyperproliferative skin diseases, such as psoriasis vulgaris. It has been implicated that the 1alpha,25-dihydroxyvitamin D3-induced differentiation of keratinocytes is mediated, at least in part, by the formation of ceramides; however, ceramides have also been identified to induce apoptosis in many cells, including keratinocytes. Therefore, it was of interest to investigate the influence of 1alpha,25-dihydroxyvitamin D3 on apoptosis in keratinocytes. Most interestingly, physiological concentrations of 1alpha,25-dihydroxyvitamin D3 did not induce apoptosis in keratinocytes, despite the formation of ceramides. Moreover, 1alpha,25-dihydroxyvitamin D3 appeared cytoprotective and made keratinocytes resistant to apoptosis induced by ceramides, ultraviolet irradiation, or tumor necrosis factor-alpha. The cytoprotective effect was accompanied by the formation of the sphingolipid breakdown product sphingosine-1-phosphate, which prevented apoptosis in analogy to 1alpha,25-dihydroxyvitamin D3. The effect of 1alpha,25-dihydroxyvitamin D3 was specific as the almost inactive precursor cholecalciferol neither induced sphingosine-1-phosphate formation nor prevented cells from apoptosis. Besides this, the cytoprotective aptitude of 1alpha,25-dihydroxyvitamin D3 was completely abolished by the sphingosine kinase inhibitor N,N-dimethylsphingosine, which blocked sphingosine-1-phosphate formation. Moreover, sphingosine-1-phosphate was able to restore the cytoprotective effect of 1alpha,25-dihydroxyvitamin D3 in the presence of N,N-dimethylsphingosine. Taken together, here we report for the first time that 1alpha,25-dihydroxyvitamin D3 protects keratinocytes from apoptosis and additionally this cytoprotection is mediated via the formation of sphingosine-1-phosphate.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects*
  • Calcitriol / pharmacology*
  • Cell Division / drug effects
  • Cell Survival / drug effects
  • Cells, Cultured
  • Ceramides / metabolism
  • Ceramides / pharmacology
  • Cytoprotection
  • Humans
  • Hydroxycholecalciferols
  • Keratinocytes / cytology
  • Keratinocytes / drug effects*
  • Keratinocytes / pathology
  • Keratinocytes / physiology*
  • Keratinocytes / radiation effects
  • Lysophospholipids*
  • Necrosis
  • Phosphotransferases (Alcohol Group Acceptor) / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Sphingosine / analogs & derivatives*
  • Sphingosine / biosynthesis*
  • Sphingosine / pharmacology
  • Sphingosine / physiology
  • Tumor Necrosis Factor-alpha / pharmacology
  • Ultraviolet Rays

Substances

  • Ceramides
  • Hydroxycholecalciferols
  • Lysophospholipids
  • Proto-Oncogene Proteins c-bcl-2
  • Tumor Necrosis Factor-alpha
  • sphingosine 1-phosphate
  • Phosphotransferases (Alcohol Group Acceptor)
  • sphingosine kinase
  • Calcitriol
  • N,N-dimethylsphingosine
  • Sphingosine
  • alfacalcidol