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首页> 外文期刊>Journal of Cellular Physiology >Vitamin D Induces Cyclooxygenase 2 Dependent Prostaglandin E-2 Synthesis in HaCaT Keratinocytes
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Vitamin D Induces Cyclooxygenase 2 Dependent Prostaglandin E-2 Synthesis in HaCaT Keratinocytes

机译：维生素D引发环氧酶2的依赖前列腺素在HaCaT依照合成角化细胞

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The active metabolite of vitamin D calcitriol and its analogs are well-known for their anti-inflammatory action in the skin, while their main side effect associated with topical treatment of inflammatory disorders is irritant contact dermatitis. Prostaglandin E-2 (PGE(2)) is pro-inflammatory at the onset of inflammation and anti-inflammatory at its resolution. We hypothesized that induction of PGE2 synthesis by calcitriol in epidermal keratinocytes may contribute both to its pro-inflammatory and anti-inflammatory effects on the skin. Treatment of human immortalized HaCaT keratinocytes with calcitriol (3-100 nM, 2-24 h) increased PGE(2) production due to increased mRNA and protein expression of COX-2, but not to increase of COX-1 or release of arachidonic acid. The effect of calcitriol on COX-2 mRNA was observed also in primary human keratinocytes. The increase in COX-2 mRNA is associated with COX-2 transcript stabilization. Calcitriol exerts this effect by a rapid (2 h) and protein synthesis independent mode of action that is dependent on PKC and Src kinase activities. Treatment with a COX-2 inhibitor partially prevented the attenuation of the keratinocyte inflammatory response by calcitriol. We conclude that upregulation of COX-2 expression with the consequent increase in PGE(2) synthesis may be one of the mechanisms explaining the Janus face of calcitriol as both a promoter and attenuator of cutaneous inflammation. (C) 2015 Wiley Periodicals, Inc.
机译：骨化三醇,维生素D的活性代谢物其类似物是众所周知的抗炎作用在皮肤上,而他们的主要与局部相关的副作用治疗炎症性疾病是刺激物接触性皮炎。出现炎症和炎性抗炎的决议。假设归纳PGE2合成的骨化三醇在表皮角化细胞其促炎和贡献抗炎作用在皮肤上。人类永生的HaCaT角质细胞骨化三醇(3 - 100海里,2-24 h)增加了铂族元素(2)生产由于信使rna和蛋白质的增加cox - 2的表达,但不是COX-1的增加或花生四烯酸的释放。骨化三醇对cox - 2 mRNA观察也在主要人类角质细胞。cox - 2 mRNA与cox - 2记录相关联稳定。快速独立(2 h)和蛋白质合成作用方式依赖于PKC和Src激酶活动。抑制剂部分阻止的衰减角化细胞的炎症反应骨化三醇。cox - 2表达随之增加铂族元素(2)合成可能的机制之一解释骨化三醇为的另一面启动子和皮肤的衰减器炎症。

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