Vitamin D protects keratinocytes from apoptosis induced by osmotic shock, oxidative stress, and tumor necrosis factor
Vitamin D protects keratinocytes from apoptosis induced by osmotic shock, oxidative stress, and tumor necrosis factor
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DOI：
10.1196/annals.1299.064
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发表时间：
2003-01-01
期刊：
影响因子：
--
通讯作者：
Ravid, A
中科院分区：
文献类型：
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作者：
Diker-Cohen, T;Koren, R;Ravid, A
骨化三醇是维生素D的激素形式，可抑制暴露于高渗、氧化应激、热休克和炎性细胞因子肿瘤坏死因子的HaCaT角质形成细胞中caspase-3样活化。该激素还保护细胞免受高渗和氧化应激诱导的caspase非依赖性细胞死亡。对高渗应激的保护作用不受EGF受体、ERK或PI13通路抑制剂的影响，也不是由于促凋亡的p38 MAP激酶活性降低所致。这些结果与之前的体内研究结果一致，即维生素D可以保护表皮角质形成细胞免受紫外线辐射或化疗所致的细胞凋亡。
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.