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首页> 外文期刊>Biology Open >Apolipoprotein CIII regulates lipoprotein-associated phospholipase A2 expression via the MAPK and NFκB pathways
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Apolipoprotein CIII regulates lipoprotein-associated phospholipase A2 expression via the MAPK and NFκB pathways

机译：载脂蛋白CIII通过MAPK和NFκB途径调节脂蛋白相关磷脂酶A2的表达

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摘要

Apolipoprotein CIII (apo CIII), a small glycoprotein that binds to the surfaces of certain lipoproteins, is associated with inflammatory and atherogenic responses in vascular cells. Lipoprotein-associated phospholipase A2 (Lp-PLA2) has been proposed as an inflammatory biomarker and potential therapeutic target for cardiovascular disease (CVD). Here, we report that apo CIII increases Lp-PLA2 mRNA and protein levels in dose- and time- dependent manner in human monocytic THP-1 cells, and the increase can be abolished by MAPK and NFκB pathway inhibitors. Lp-PLA2 inhibitor, 1-linoleoyl glycerol attenuates the inflammation induced by apo CIII. In turn, exogenous Lp-PLA2 expression upregulates apo CIII and the upregulation can be inhibited by 1-linoleoyl glycerol in HepG2 cells. Moreover, plasma Lp-PLA2 level is correlated with apo CIII expression in pig liver. In vivo , Lp-PLA2 expression in monocytes and its activity in serum were significantly increased in human apo CIII transgenic porcine models compared with wild-type pigs. Our results suggest that Lp-PLA2 and apo CIII expression level is correlated with each other in vitro and in vivo .
机译：载脂蛋白CIII（载脂蛋白CIII）是一种与某些脂蛋白表面结合的小糖蛋白，与血管细胞的炎症反应和动脉粥样硬化反应有关。脂蛋白相关的磷脂酶A2（Lp-PLA2）已被提出作为炎症生物标志物和心血管疾病（CVD）的潜在治疗靶标。在这里，我们报道载脂蛋白CIII以剂量和时间依赖性方式在人单核细胞THP-1细胞中增加Lp-PLA2 mRNA和蛋白水平，并且MAPK和NFκB途径抑制剂可以消除这种增加。 Lp-PLA2抑制剂1-亚油酰甘油可减轻Apo CIII诱导的炎症。反过来，外源性Lp-PLA2表达上调apo CIII，并且该上调可以被HepG2细胞中的1-亚油酰甘油抑制。此外，血浆Lp-PLA2水平与猪肝中载脂蛋白CIII表达相关。在体内，与野生型猪相比，人apo CIII转基因猪模型中Lp-PLA2在单核细胞中的表达及其在血清中的活性显着增加。我们的结果表明，Lp-PLA2和载脂蛋白CIII的表达水平在体内和体外相互关联。

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