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结合性组织生长因子是血管激素II诱导纤维化的一个媒介

Mónica Rupérez¹, Oscar Lorenzo, Luis Miguel Blanco-Colio

¹Vascular and Renal Research Laboratory, Autónoma University, Fundación Jiménez Díaz, Avda Reyes Católicos, 2, 28040 Madrid, Spain.

|September 4, 2003

概括

ангиотензин II (Ang II) 在血管细胞中显著增加结缔组织生长因子 (CTGF),这表明CTGF介导Ang II.

科学领域:

血管生物学血管生物学
纤维化研究纤维化研究
分子医学是分子医学.

背景情况:

ангиотензин II (Ang II) 与血管损伤和纤维化有关.
结合组织生长因子 (CTGF) 是一种新发现的纤维化介质.
在血管纤维化中Ang II和CTGF之间的关系以前未被探索.

研究的目的:

调查 ангиотензин II (Ang II) 和结缔组织生长因子 (CTGF) 之间的潜在联系.
为了确定Ang II是否影响血管细胞中CTGF表达.
探索CTGF作为Ang II诱导的血管益纤维效应中介者的作用.

主要方法:

在体内研究涉及系统性Ang II输液给大鼠,免疫组织化学用于评估CTGF和细胞外矩阵 (ECM) 蛋白质表达.
在体外研究中,使用Ang II治疗的血管光滑肌细胞,分析CTGFmRNA和蛋白质表达.
使用AT1受体对抗剂和CTGF反感性寡核酸来阻断Ang II效应.

主要成果:

系统性Ang II输液给大鼠导致大动脉中CTGF和ECM蛋白的表达增加,而AT1抗剂可以逆转这些效应.
在体外,Ang II迅速诱导了血管光滑肌细胞中的CTGFmRNA和蛋白质的产生,而这些细胞被AT1抗剂阻断.
细胞内信号通路包括蛋白激酶C,活性氧物种和TGF-β都参与了Ang II诱导的CTGF合成.

结论:

ангиотензин II (Ang II),通过AT1受体起作用,在血管细胞中调节连接组织生长因子 (CTGF).
这项研究确立了CTGF作为Ang II在血管疾病中的益纤维化作用的新型调解者.
研究结果表明,准Ang II-CTGF通路可能是血管纤维化治疗的治疗策略.

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