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Collagen and Elastin Degradation by Matrix Metalloproteinases and Tissue Inhibitors of Matrix Metalloproteinases in Acute Aortic Dissection and Atherosclllerotic Aneurysm.

急性主动脉夹层和动脉粥样硬化性动脉瘤中基质金属蛋白酶和基质金属蛋白酶组织抑制剂对胶原蛋白和弹性蛋白的降解。

基本信息

批准号：
10670178
负责人：
ISHII Toshiharu
金额：
$ 1.66万
依托单位：
School of Medicine,Toho University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10670178/
关键词：
Acute Aortic Dissection Collagen Elastin MMP TIMP 弾性線維 TIMP dissecting aneurysm matrix metalloproteinare Tissue inhibitor of MMP collagen elastin

项目摘要

Degradation process of collagen and elastin in acute aortic dissection (AAD) has been ultra-structurally and immunohistochemically investigated with matrix metalloproteinase s(MMPs)-1, 2, 3 amd-9, and their counterparts of tissue inhibitors of matrix metalloproteinases (TIMPs)-1 and -2. The results at entry site(ES) of dissection were compared with those at fully remote site from ES(RS) and ascending aortas from age-sex matched control cases. By electron microscopy on disscted media, spirally thickened collagen with usual banding pattern were con-currently noted together with normal collagen and elastin often exhibiting fragmentation or disruption. In addition, basement membrane surrounding cytoplasm of smooth muscle cells(SMCs) comprising media was frequently thinned or lost at such circumstances. These findings were only rarely shown in the aortic walls at RS in AAD cases, not only the expression of MMP-1 was significantly distinct in SMC cytoplasm of both intima and media, but also significant expression of MMP-2 and -9 was recognized in intoma, when compared with those expressions at RS in AAD cases and at ascending aortas of controls. Significant expression of TIMP-1 and -2 was correspondingly demonstrated at ES in AAD cases, when compared with that at RS in AAD cases and at ascending aorta of controls. These findings suggest that both degradation of collagen and elastin and occurrence of AAD do not incidentally take place, rather AAD is induced by the preceding alterations of those extracellular matrices caused by alterations of SMCs at vulnerable segment of ascending aorta through hemodynamic stress, which is further mediated by hypertension.

应用基质金属蛋白酶（MMPs）-1，2，3和9及其相应的基质金属蛋白酶组织抑制剂（TIMPs）-1和-2对急性主动脉夹层（AAD）中胶原和弹性蛋白的降解过程进行了超微结构和免疫组化研究。将解剖入路部位（ES）的结果与年龄性别匹配的对照组病例中完全远离ES的部位（RS）和升主动脉的结果进行比较。电镜下可见正常胶原和弹性蛋白断裂或断裂，同时可见正常胶原和弹性蛋白呈正常带型增厚。此外，在这种情况下，包含中膜的平滑肌细胞（SMC）的细胞质周围的基底膜经常变薄或丢失。MMP-1在主动脉内膜和中膜SMC胞浆中的表达明显高于对照组，MMP-2和MMP-9在内膜瘤中的表达也明显高于对照组。AAD患者ES处TIMP-1和TIMP-2的表达明显高于AAD患者RS处和对照组升主动脉处。这些结果表明，胶原和弹性蛋白的降解和AAD的发生不是偶然发生的，而是通过血流动力学应激引起的升主动脉易损段SMC的改变引起的这些细胞外基质的改变而诱导的，这种改变进一步由高血压介导。