Kallistatin correlates with inflammation in abdominal aortic aneurysm and suppresses its formation in mice

Kallistatin correlates with inflammation in abdominal aortic aneurysm and suppresses its formation in mice
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DOI:
10.21037/cdt.2019.12.08
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发表时间:
2020-04-01
影响因子:
2.4
通讯作者:
Zhan, Jian
Zhan, Jian
中科院分区:
医学4区
文献类型:
--
作者:
He, Yuchen;Han, Yanshuo;Zhan, Jian

文献摘要

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背景:由丝氨酸蛋白酶抑制剂4编码的激肽释放酶抑制剂(KS)被认为在许多心血管疾病中起保护作用。然而,其在腹主动脉瘤(AAA)发病机制中的作用仍不清楚。本研究的目的是探讨KS与AAA pathogenicity.Methods的潜在关联:我们检测KS(SERPINA 4)在人AAA中的表达,通过PCR,免疫组化,蛋白质印迹,酶联免疫吸附试验(ELISA)和分析Kallistain和临床数据之间的相关性。然后,我们分析了重组KS对血管紧张素II(AngII)输注给载脂蛋白E缺陷(ApoE(-/-))小鼠建立的小鼠AAA模型中AAA形成和Wingless(Wnt)信号通路的影响。
Background: Kallistatin (KS), encoded by SERPINA4, was suggested to play a protective role in many cardiovascular diseases. However, its role in the pathogenesis of abdominal aortic aneurysm (AAA) remains unclear. The aim of this study was to examine the potential association of KS with AAA pathogenesis.Methods: We examined KS (SERPINA4) expression in human AAA by PCR, immunohistochemistry, western blotting, and enzyme-linked immunosorbent assay (ELISA) and analyzed correlations between kallistain and clinical data. We then analyzed the effect of recombinant KS on AAA formation and the Wingless (Wnt) signaling pathway in a mouse AAA model developed by angiotensin II (AngII) infusion to apolipoprotein E-deficient (ApoE(-/-)) mice.Results: In AAA tissue samples, KS was significantly increased compared with samples from the control group (P