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Updated: Aug 25, 2026

Isolation and Culture of Primary Mouse Keratinocytes from Neonatal and Adult Mouse Skin
Published on: July 14, 2017
Vitamin D protects keratinocytes from apoptosis induced by osmotic shock, oxidative stress, and tumor necrosis factor
Talia Diker-Cohen1, Ruth Koren, Uri A Liberman
1Department of Physiology and Pharmacology, Felsenstein Medical Research Center, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
Abstract:
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.
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