caveolin-1 基因缺失小鼠巨噬细胞中花生四烯酸分布改变导致环氧合酶产物合成减少。
Altered arachidonate distribution in macrophages from caveolin-1 null mice leading to reduced eicosanoid synthesis.
机构信息
Instituto de Biología y Genética Molecular, Consejo Superior de Investigaciones Científicas, 47003 Valladolid, Spain.
出版信息
J Biol Chem. 2011 Oct 7;286(40):35299-307. doi: 10.1074/jbc.M111.277137. Epub 2011 Aug 17.
Abstract
In this work we have studied the effect of caveolin-1 deficiency on the mechanisms that regulate free arachidonic acid (AA) availability. The results presented here demonstrate that macrophages from caveolin-1-deficient mice exhibit elevated fatty acid incorporation and remodeling and a constitutively increased CoA-independent transacylase activity. Mass spectrometry-based lipidomic analyses reveal stable alterations in the profile of AA distribution among phospholipids, manifested by reduced levels of AA in choline glycerophospholipids but elevated levels in ethanolamine glycerophospholipids and phosphatidylinositol. Furthermore, macrophages from caveolin-1 null mice show decreased AA mobilization and prostaglandin E(2) and LTB(4) production upon cell stimulation. Collectively, these results provide insight into the role of caveolin-1 in AA homeostasis and suggest an important role for this protein in the eicosanoid biosynthetic response.
摘要
在这项工作中，我们研究了窖蛋白-1 缺失对调节游离花生四烯酸 (AA) 可用性的机制的影响。这里呈现的结果表明，窖蛋白-1 缺失的小鼠巨噬细胞表现出脂肪酸掺入和重塑增加，以及组成型增加的辅酶 A 非依赖性转酰基酶活性。基于质谱的脂质组学分析揭示了 AA 在磷脂中的分布特征的稳定改变，表现为胆碱甘油磷脂中的 AA 水平降低，但乙醇胺甘油磷脂和磷脂酰肌醇中的 AA 水平升高。此外，窖蛋白-1 缺失的小鼠巨噬细胞在细胞刺激时表现出 AA 动员和前列腺素 E(2)和 LTB(4)产生减少。总的来说，这些结果提供了对窖蛋白-1 在 AA 动态平衡中的作用的深入了解，并表明该蛋白在类二十烷酸生物合成反应中起着重要作用。
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