1999 Fiscal Year Final Research Report Summary
Collagen and Elastin Degradation by Matrix Metalloproteinases and Tissue Inhibitors of Matrix Metalloproteinases in Acute Aortic Dissection and Atherosclllerotic Aneurysm.
| Project/Area Number |
10670178
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Human pathology
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| Research Institution | School of Medicine,Toho University |
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Principal Investigator |
ISHII Toshiharu Second Department of Pathology, School of Medicine, Toho University, Professor, 医学部, 教授 (30101893)
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| Co-Investigator(Kenkyū-buntansha) |
AKASAKA Yoshikiyo Second Department of Pathology, School of Medicine, Toho University, Associate Professor, 医学部, 助教授 (60202511)
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| Project Period (FY) |
1998 – 1999
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| Keywords | Acute Aortic Dissection / Collagen / Elastin / MMP / TIMP |
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| Research Abstract |
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.
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Research Products
(6 results)
