Elevation of ADAM10, ADAM17, MMP-2 and MMP-9 expression with media degeneration features CaCl2-induced thoracic aortic aneurysm in a rat model
Elevation of ADAM10, ADAM17, MMP-2 and MMP-9 expression with media degeneration features CaCl2-induced thoracic aortic aneurysm in a rat model
复制标题
大鼠模型中 ADAM10、ADAM17、MMP-2 和 MMP-9 表达升高并伴有介质变性特征 CaCl2 诱导的胸主动脉瘤
DOI：
10.1016/j.yexmp.2010.05.006
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发表时间：
2010-08-01
影响因子：
3.6
通讯作者：
Shen, Weifeng
中科院分区：
文献类型：
--
作者：
Geng, Liang;Wang, Wei;Shen, Weifeng
目的：建立氯化钙(CaCl2)致大鼠胸主动脉瘤(TAA)模型，探讨去整合素和金属蛋白酶(ADAM)、基质金属蛋白酶(MMPs)及其内源性抑制物(TIMPs)在TAA形成中的作用。12周后处死动物，收集CaCl2处理组、CaCl2组(n=12)和氯化钠组(n=12)的主动脉节段，进行组织学和分子生物学评价。结果：尽管CaCl2处理的节段、非CaCl2处理的节段和氯化钠处理的节段的外径相似，但CaCl2处理的节段出现动脉瘤样改变(n=6，50%)，中层变性伴局部断裂，弹性纤维断裂，胶原沉积增加(n=12,100%)。CaCl2处理的节段中，MMP2、MMP9、ADAM-10和ADAM-17mRNA的表达均升高(均P
Purpose: This study was designed to establish a rat model of thoracic aortic aneurysm (TAA) by calcium chloride (CaCl2)-induced arterial injury and to explore the potential role of a disintegrin and metalloproteinase (ADAM), matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) in TAA formation.Methods: Thoracic aorta of male Sprague-Dawley rats was exposed to 0.5 M CaCl2 or normal saline (NaCl). After 12 weeks, animals were euthanized, and CaCl2-treated, CaCl2-untreated (n = 12) and NaCl-treated aortic segments (n = 12) were collected for histological and molecular assessments. MMP-TIMP and ADAM mRNAs were semi-quantitatively analyzed and protein expressions were determined by immunohistochemistry.Results: Despite similar external diameters among CaCl2-treated, non-CaCl2-treated and NaCl-treated segments, aneurymal alteration (n = 6, 50%), media degeneration with regional disruption, fragmentation of elastic fiber, and increased collagen deposition (n = 12, 100%) were demonstrated in CaCl2-treated segments. MMP-2, MMP-9, ADAM-10 and ADAM-17 mRNA levels were increased in CaCl2-treated segments (all p