Activated forms of MMP2 and MMP9 in abdominal aortic aneurysms,☆☆,,★★,

A preliminary report of this manuscript was presented at the XXIst World Congress of the International Society for Cardiovascular Surgery, Lisbon, Portugal, Sept. 12-15, 1993.
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Abstract

Purpose: The consistent observation of a reduction of the elastin concentration in abdominal aortic aneurysms (AAAs) has led us to investigate in AAA specimens two metalloproteinases that display elastase activity, MMP2 (gelatinase A/72 kDa) and MMP9 (gelatinase B/92 kDa).

Methods: Samples of full-thickness aortic wall, adherent thrombus, and serum were collected in 10 patients with AAAs. Samples of normal aortic wall and serum were taken from 6 age-matched control patients. Quantitative gelatin-zymography and gelatinolytic soluble assays after acetyl-phenyl mercuric acid activation were performed on serum and tissue extracts, and the results were expressed in units on a comparative wet-weight basis. Histologic analysis was performed in parallel to score the inflammatory infiltrate.

Results: The luminal and parietal parts of the thrombus contained, respectively, 20- and 10-fold more gelatinolytic activity than the serum. The predominate form was MMP9. Although the total gelatinolytic activity was in the same range both in AAAs and in normal walls, a significantly higher proportion of MMP9 was found in the aneurysmal aortic walls. Furthermore, a significant proportion of MMP9 was under its processed active form, which was never observed in normal samples. A significantly higher proportion of MMP2 was also present as processed active form in AAA wall. This latter parameter positively correlated with the inflammatory score.

Conclusions: The presence of activated MMP9 and MMP2 might contribute to the degradation of the extracellular matrix proteins that occurs during the development of aneurysms. (J Vasc Surg 1996;24:127-33.)

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From the Department of Cardiovascular Surgery (Drs. Sakalihasan and Limet), the Department of Anatomopathology (Dr. Delvenne), and Laboratory of Connective Tissues Biology (Drs. Nusgens and Lapiere), CHU Sart Tilman, University of Liège.

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Supported in part by the “Fonds de Recherche de la Faculté de Médecine” of the University of Liège, the “Actions de Recherche Concertée 90-94/139” of the French Community of Belgium and a grant from the Belgian “Fonds de Recherche Scientifique Médicale, |mx3.4529.95.

Reprint requests: Charles M. Lapière, Laboratory of Connective Tissues Biology, Tour de Pathologie, B23, B-4000 Sart Tilman, Belgium.

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