Apolipoprotein E-deficient rats develop atherosclerotic plaques in partially ligated carotid arteries

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• 作者：Shujie Wei¹ ; Yan Zhang¹ ; Linan Su ; Kecheng He ; Qiang Wang ; Yunrong Zhang ; Dachun Yang ; Yongjian Yang ; ^{yangyongjian38@sina.com" class="auth_mail" title="E-mail the corresponding author} ; Shuangtao Ma ; ^{ma.shuangtao@gmail.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：ApoE ; TLEN ; Knockout ; Atherosclerosis
• 刊名：Atherosclerosis
• 出版年：2015
• 出版时间：December 2015
• 年：2015
• 卷：243
• 期：2
• 页码：589-592
• 全文大小：1479 K

文摘

The goal of this study was to establish an apolipoprotein E-deficient (ApoE^-/-) rat model.

Methods

The ApoE^-/- rat was created by TALEN-mediated gene targeting in the genetic background of Sprague Dawley rat. Six-to eight-week-old male rats were used in the experiments (n = 10 in each group).

Results

After fed with high-cholesterol diet (HCD) for 12 weeks, the ApoE^-/- rats displayed typical dyslipidemia. In contrast, HCD failed to induce hypercholesterolemia in wild-type rats. However, there was no obvious atherosclerotic lesion in oil red O-stained en face aortas and the aortic root sections in both genetic types of rats. Interestingly, partial ligation caused the formation of plaques consist of lipid and macrophages in carotid arteries from ApoE^-/- rats, but induced the neointimal hyperplasia in wild-type rats. Additionally, we found that HCD slightly increased the expression of adhesion molecules, while partial ligation dramatically upregulated these molecules.

Conclusions

The ApoE^-/- rat is a novel model for dyslipidemia and could also be used in the research of atherosclerosis.