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Expression of matrix metalloproteinases and endogenous Inhibitors in abdominal aortic aneurysm and aortoiliac occlusive disease (syndrome Leriche)
N. Vasic, S. Glumac, S. Pejic, LJ. Amidzic, LJ. Tadic Latinovic, B. Dozic, S. Hinic, Z. Maksimovic
Language English Country Czech Republic
Document type Journal Article
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ProQuest Central
from 2005-01-01
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- 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
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.
Clinic for Vascular and Endovascular Surgery Serbian Clinical Centre
Department of Cardiology University Clinical Hospital Centre Bezanijska kosa
Department of Clinical Pathology
Department of Vascular Surgery
Institute of Pathology School of Dental Medicine University Clinical Hospital Centre Bezanijska kosa
Institute of Pathology School of Medicine University Clinical Hospital Centre Bezanijska kosa
University Clinical Centre of the Republic of Srpska Banja Luka Bosnia and Herzegovina
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- $a 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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