Expression of Matrix Metalloproteinases and Endogenous Inhibitors in Abdominal Aortic Aneurysm and Aortoiliac Occlusive Disease (Syndrome Leriche)
Language English Country Czech Republic Media print
Document type Journal Article
PubMed
29687775
DOI
10.14712/fb2017063050209
PII: file/5858/fb2017a0029.pdf
Knihovny.cz E-resources
- MeSH
- Aortic Aneurysm, Abdominal metabolism MeSH
- Arterial Occlusive Diseases metabolism MeSH
- Immunohistochemistry MeSH
- Humans MeSH
- Matrix Metalloproteinase 9 metabolism MeSH
- Matrix Metalloproteinases metabolism MeSH
- Myocytes, Smooth Muscle metabolism MeSH
- Aortic Diseases metabolism MeSH
- Tissue Inhibitor of Metalloproteinase-1 metabolism MeSH
- Tissue Inhibitor of Metalloproteinase-2 metabolism MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Matrix Metalloproteinase 9 MeSH
- Matrix Metalloproteinases MeSH
- Tissue Inhibitor of Metalloproteinase-1 MeSH
- Tissue Inhibitor of Metalloproteinase-2 MeSH
Matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) play a complex role in the pathogenesis of atherosclerosis. We compared (1) the histopathological findings in patients with abdominal aortic aneurysms (AAA) and aortoiliac occlusive disease (AOD); (2) the expression of MMP-2/MMP-9 and TIMP-1/TIMP-2 in aortic layers, inflammatory cells and smooth muscle cells (SMCs), aiming to identify the common underlying pathogenic mechanisms of the disease development. Samples were obtained from 30 patients with AAA and 30 with AOD. Aortic histology and immunohistochemistry were performed to evaluate inflammatory changes and MMP and TIMP expression. Thrombosis and ulceration were more frequent in AOD than in AAA. The MMP-9 expression was elevated in all aortic layers of AAA patients and in media/adventitia of AOD patients, mainly followed by lower expression of its inhibitor TIMP-1. Higher MMP-9 expression was also found in SMCs and macrophages of both AAA and AOD specimens, while higher TIMP-1/TIMP-2 were predominantly observed in the lymphocytes and macrophages of the aneurysm. These results showed that both conditions exhibited increased MMP-9 expression; however, the MMP expression pattern differed to some degree between the aneurysms and occlusive disease. The variations in molecular mechanisms underlying dilatative/stenosing disease warrant further investigation.
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