Vitamin D protects keratinocytes from apoptosis induced by osmotic shock, oxidative stress, and tumor necrosis factor.
Calcitriol, the hormonal form of vitamin D, inhibited caspase-3-like activation in HaCaT keratinocytes exposed to hyperosmotic and oxidative stresses, heat shock, and the inflammatory cytokine TNF. The hormone also protected the cells from caspase-independent cell death induced by hyperosmotic and oxidative stresses. The protection against hyperosmotic stress is not affected by inhibitors of the EGF receptor, ERK or PI13 kinase pathways, neither is it due to reduced activity of the proapoptotic p38 MAP kinase. These results are in accordance with previous in vivo findings that vitamin D protects epidermal keratinocytes from apoptosis due to UV radiation or chemotherapy.
Diker-Cohen
Talia
T
Department of Physiology and Pharmacology, Felsenstein Medical Research Center, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
Koren
Ruth
R
Liberman
Uri A
UA
Ravid
Amiram
A
D002117:Calcitriol / Q000494:pharmacology*; D053148:Caspase 3; D061945:Caspase Inhibitors; D016923:Cell Death / Q000187:drug effects; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D004789:Enzyme Activation / Q000187:drug effects; D006801:Humans; D007223:Infant; D015603:Keratinocytes / Q000166:cytology* / Q000187:drug effects / Q000502:physiology*; D018384:Oxidative Stress; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
D061945:Caspase Inhibitors; D014409:Tumor Necrosis Factor-alpha; C505407:CASP3 protein, human; D053148:Caspase 3; D002117:Calcitriol