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首页> 外文期刊>Cell metabolism >Reduced apoptosis and plaque necrosis in advanced atherosclerotic lesions of Apoe-/- and Ldlr-/- mice lacking CHOP.
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Reduced apoptosis and plaque necrosis in advanced atherosclerotic lesions of Apoe-/- and Ldlr-/- mice lacking CHOP.

机译：缺乏CHOP的Apoe-/-和Ldlr-/-小鼠晚期动脉粥样硬化病变中的凋亡减少和斑块坏死减少。

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摘要

Endoplasmic reticulum (ER) stress is a hallmark of advanced atherosclerosis, but its causative role in plaque progression is unknown. In vitro studies have implicated the ER stress effector CHOP in macrophage apoptosis, a process involved in plaque necrosis in advanced atheromata. To test the effect of CHOP deficiency in vivo, aortic root lesions of fat-fed Chop+/+;Apoe-/- and Chop-/-;Apoe-/- mice were analyzed for size and morphology. Despite similar plasma lipoproteins, lesion area was 35% smaller in Chop-/-;Apoe-/- mice. Most importantly, plaque necrosis was reduced by approximately 50% and lesional apoptosis by 35% in the CHOP-deficient mice. Similar results were found in fat-fed Chop-/-;Ldlr-/- versus Chop+/+;Ldlr-/- mice. Thus, CHOP promotes plaque growth, apoptosis, and plaque necrosis in fat-fed Apoe-/- and Ldlr-/- mice. These data provide direct evidence for a causal link between the ER stress effector CHOP and plaque necrosis and suggest that interventions weakening this arm of the UPR may lessen plaque progression.
机译：内质网应激是晚期动脉粥样硬化的标志，但其在斑块进展中的致病作用尚不清楚。体外研究表明，ER应激效应因子CHOP参与了巨噬细胞凋亡，该过程涉及晚期动脉粥样斑块坏死。为了测试体内CHOP缺乏症的影响，对脂肪喂养的Cop + / +; Apoe-/-和Chop-/-; Apoe-/-小鼠的主动脉根部病变的大小和形态进行了分析。尽管血浆脂蛋白相似，但是Chop-/-; Apoe-/-小鼠的病变面积小了35％。最重要的是，在CHOP缺陷型小鼠中，斑块坏死减少了约50％，病灶凋亡减少了35％。在用脂肪喂养的Chop-/-; Ldlr-/-与Chop + / +; Ldlr-/-小鼠中发现了相似的结果。因此，CHOP促进了脂肪喂养的Apoe-/-和Ldlr-/-小鼠的斑块生长，细胞凋亡和斑块坏死。这些数据为内质网应激反应效应因子CHOP和斑块坏死之间的因果关系提供了直接证据，并表明弱化UPR这一臂的干预措施可能会减少斑块进展。

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