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血小板激活因子通过花生四烯酸非选择性磷脂酶 A2 刺激分化角质形成细胞释放花生四烯酸。

Platelet activating factor stimulates arachidonic acid release in differentiated keratinocytes via arachidonyl non-selective phospholipase A2.

机构信息

Department of Biology, Norwegian University of Science and Technology, NTNU, Trondheim, Norway.

出版信息

Arch Dermatol Res. 2010 Apr;302(3):221-7. doi: 10.1007/s00403-009-1017-8. Epub 2009 Dec 30.

Abstract

Platelet activating factor (PAF, 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) is known to be present in excess in psoriatic skin, but its exact role is uncertain. In the present study we demonstrate for the first time the role of group VI PLA(2) in PAF-induced arachidonic acid release in highly differentiated human keratinocytes. The group IValpha PLA(2) also participates in the release, while secretory PLA(2)s play a minor role. Two anti-inflammatory synthetic fatty acids, tetradecylthioacetic acid and tetradecylselenoacetic acid, are shown to interfere with signalling events upstream of group IValpha PLA(2) activation. In summary, our major novel finding is the involvement of the arachidonyl non-selective group VI PLA(2) in PAF-induced inflammatory responses.

摘要

血小板激活因子 (PAF,1-O-烷基-2-乙酰-sn-甘油-3-磷酸胆碱) 已知在银屑病皮肤中过量存在,但确切作用尚不确定。在本研究中,我们首次证明了组 VI PLA(2) 在高度分化的人角质形成细胞中 PAF 诱导的花生四烯酸释放中的作用。IValpha PLA(2) 也参与了释放,而分泌型 PLA(2) 则起次要作用。两种抗炎合成脂肪酸,十四烷基硫代乙酸和十四烷基硒代乙酸,被证明可以干扰 IValpha PLA(2) 活化上游的信号事件。总之,我们的主要新发现是参与了 PAF 诱导的炎症反应的花生四烯酸非选择性组 VI PLA(2)。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97c0/2829133/a740a55e3cd4/403_2009_1017_Fig1_HTML.jpg

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