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培养的小鼠角质形成细胞中的花生四烯酸代谢

Arachidonic acid metabolism in cultured mouse keratinocytes.

作者信息

Kondoh H, Sato Y, Kanoh H

出版信息

J Invest Dermatol. 1985 Jul;85(1):64-9. doi: 10.1111/1523-1747.ep12275349.

DOI:10.1111/1523-1747.ep12275349
PMID:3925027
Abstract

We attempted to characterize the general features of arachidonate metabolism in cultured mouse keratinocytes. The cells labeled with [3H]arachidonate were stimulated by 12-O-tetradecanoylphorbol-13-acetate (TPA), ionophore A23187, and fetal bovine serum (FBS). Common to the three substances, phosphatidylinositol, phosphatidylethanolamine, and phosphatidylcholine almost equally served as sources of arachidonate liberated by the action of phospholipase A2. The stimulation of phospholipase A2 action was observed in the order of A23187 greater than FBS greater than TPA. When stimulated by TPA or A23187, the radioactivity released into the extracellular medium was mostly found in prostaglandin (PG) E2. Formation of other PGs and hydroxyeicosatetraenoate (HETE) was extremely limited. In the case of stimulation by FBS, however, the released radioactivity was mainly associated with non-converted arachidonate. FBS also inhibited the TPA- and A23187-induced conversion of arachidonate to PGE2. Phospholipid degradation induced by the three stimulators was similarly dependent on extracellular Ca2+. The stimulation by FBS and A23187 was suppressed by calmodulin antagonists, though the effect of A23187 was much more sensitive to the antagonists when compared to that of FBS. We observed more than additive effects of the three stimulators when tested together.

摘要

我们试图描述培养的小鼠角质形成细胞中花生四烯酸代谢的一般特征。用[3H]花生四烯酸标记的细胞分别用12-O-十四烷酰佛波醇-13-乙酸酯(TPA)、离子载体A23187和胎牛血清(FBS)刺激。这三种物质的共同之处在于,磷脂酰肌醇、磷脂酰乙醇胺和磷脂酰胆碱几乎同样作为磷脂酶A2作用释放的花生四烯酸的来源。观察到磷脂酶A2作用的刺激顺序为A23187大于FBS大于TPA。当受到TPA或A23187刺激时,释放到细胞外培养基中的放射性主要存在于前列腺素(PG)E2中。其他PG和羟基二十碳四烯酸(HETE)的形成极其有限。然而,在FBS刺激的情况下,释放的放射性主要与未转化的花生四烯酸相关。FBS还抑制TPA和A23187诱导的花生四烯酸向PGE2的转化。三种刺激剂诱导的磷脂降解同样依赖于细胞外Ca2+。FBS和A23187的刺激被钙调蛋白拮抗剂抑制,尽管与FBS相比,A23187对拮抗剂的作用更敏感。当一起测试时,我们观察到三种刺激剂的作用超过相加效应。

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