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脂联素可减轻高脂血症小鼠腹主动脉瘤的形成。

Adiponectin attenuates abdominal aortic aneurysm formation in hyperlipidemic mice.

作者信息

Yoshida Sumiko, Fuster José Javier, Walsh Kenneth

机构信息

Molecular Cardiology, Whitaker Cardiovascular Institute, Boston University School of Medicine, 715 Albany Street, W611, Boston, MA 02118, USA.

Molecular Cardiology, Whitaker Cardiovascular Institute, Boston University School of Medicine, 715 Albany Street, W611, Boston, MA 02118, USA.

出版信息

Atherosclerosis. 2014 Aug;235(2):339-46. doi: 10.1016/j.atherosclerosis.2014.05.923. Epub 2014 May 23.

DOI:10.1016/j.atherosclerosis.2014.05.923
PMID:24911638
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4100794/
Abstract

OBJECTIVE

Abdominal aortic aneurysms (AAA) are age-associated, life-threatening inflammatory dilations of the abdominal aorta. Human population studies have shown an association between obesity and AAA formation, but the molecular mechanisms underlying this connection remain largely unexplored. Adiponectin is an anti-inflammatory adipokine that is downregulated in obesity. In this study we evaluated the role of adiponectin in a model of AAA using apolipoprotein E/adiponectin double-knockout (Apoe(-/-)Apn(-/-)) mice.

APPROACH AND RESULTS

Angiotensin II (Ang II)-infusion in male Apoe(-/-)Apn(-/-) mice led to a higher incidence of AAA and a significant increase of maximal aortic diameter compared with that of Apoe(-/-) mice (2.12 ± 0.07 mm vs. 1.67 ± 0.09 mm, respectively at 28 days). Adiponectin deficiency augmented the early infiltration of macrophages and increased the expression of pro-inflammatory factors in the dilated aortic wall. MMP-2 and MMP-9 activation was also augmented in the aorta of Apoe(-/-)Apn(-/-) mice compared to Apoe(-/-) mice. These data suggest that the downregulation of adiponectin could directly contribute to the elevated incidence of AAA observed in obese individuals.

CONCLUSIONS

Adiponectin attenuates Ang II-induced vascular inflammation and AAA formation in mice.

摘要

目的

腹主动脉瘤（AAA）是与年龄相关的、危及生命的腹主动脉炎性扩张。人群研究表明肥胖与AAA形成之间存在关联，但这种联系背后的分子机制在很大程度上仍未被探索。脂联素是一种抗炎性脂肪因子，在肥胖状态下表达下调。在本研究中，我们使用载脂蛋白E/脂联素双敲除（Apoe(-/-)Apn(-/-)）小鼠评估了脂联素在AAA模型中的作用。

方法与结果

与Apoe(-/-)小鼠相比，雄性Apoe(-/-)Apn(-/-)小鼠输注血管紧张素II（Ang II）导致AAA发生率更高，最大主动脉直径显著增加（28天时分别为2.12 ± 0.07 mm和1.67 ± 0.09 mm）。脂联素缺乏增加了巨噬细胞的早期浸润，并增加了扩张主动脉壁中促炎因子的表达。与Apoe(-/-)小鼠相比，Apoe(-/-)Apn(-/-)小鼠主动脉中MMP-2和MMP-9的激活也增强。这些数据表明脂联素的下调可能直接导致肥胖个体中观察到的AAA发生率升高。

结论

脂联素可减轻Ang II诱导的小鼠血管炎症和AAA形成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/629a/4100794/60e82fe5a884/nihms601181f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/629a/4100794/cbe9db4e4629/nihms601181f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/629a/4100794/ba5539843cd6/nihms601181f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/629a/4100794/b7a02d23c270/nihms601181f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/629a/4100794/401eb882fca9/nihms601181f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/629a/4100794/60e82fe5a884/nihms601181f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/629a/4100794/cbe9db4e4629/nihms601181f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/629a/4100794/ba5539843cd6/nihms601181f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/629a/4100794/b7a02d23c270/nihms601181f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/629a/4100794/401eb882fca9/nihms601181f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/629a/4100794/60e82fe5a884/nihms601181f5.jpg

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