IVA组磷脂酶A(2)缺乏通过增强自噬作用来预防四氯化碳诱导的肝细胞死亡。
Group IVA phospholipase A(2) deficiency prevents CCl4-induced hepatic cell death through the enhancement of autophagy.
作者信息
Ishihara Keiichi, Kanai Shiho, Tanaka Kikuko, Kawashita Eri, Akiba Satoshi
机构信息
Department of Pathological Biochemistry, Kyoto Pharmaceutical University, Misasagi Nakauchi-cho 5, Yamashina-ku, Kyoto 607-8414, Japan.
Department of Pathological Biochemistry, Kyoto Pharmaceutical University, Misasagi Nakauchi-cho 5, Yamashina-ku, Kyoto 607-8414, Japan.
出版信息
Biochem Biophys Res Commun. 2016 Feb 26;471(1):15-20. doi: 10.1016/j.bbrc.2016.01.186. Epub 2016 Feb 3.
Group IVA phospholipase A2 (IVA-PLA2), which generates arachidonate, plays a role in inflammation. IVA-PLA2-deficiency reduced hepatotoxicity and hepatocyte cell death in mice that received a single dose of carbon tetrachloride (CCl4) without any inhibitory effects on CCl4-induced lipid peroxidation. An immunoblot analysis of extracts from wild-type mouse- and IVA-PLA2 KO mouse-derived primary hepatocytes that transiently expressed microtubule-associated protein 1 light chain 3B (LC3) revealed a higher amount of LC3-II, a typical index of autophagosome formation, in IVA-PLA2-deficient cells, suggesting the enhancement of constitutive autophagy. IVA-PLA2 may promote CCl4-induced cell death through the suppression of constitutive autophagy in hepatocytes.
IVA组磷脂酶A2（IVA-PLA2）可生成花生四烯酸，在炎症中发挥作用。在接受单剂量四氯化碳（CCl4）的小鼠中，IVA-PLA2缺乏可降低肝毒性和肝细胞死亡，且对CCl4诱导的脂质过氧化没有任何抑制作用。对野生型小鼠和IVA-PLA2基因敲除小鼠来源的原代肝细胞提取物进行免疫印迹分析，这些原代肝细胞瞬时表达微管相关蛋白1轻链3B（LC3），结果显示，在IVA-PLA2缺陷细胞中，自噬体形成的典型指标LC3-II的含量更高，这表明组成型自噬增强。IVA-PLA2可能通过抑制肝细胞中的组成型自噬来促进CCl4诱导的细胞死亡。
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