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Cardiovascular Research 1997 34(3):597-602; doi:10.1016/S0008-6363(97)00048-5
© 1997 by European Society of Cardiology
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Copyright © 1997, European Society of Cardiology

Homocysteine induces synthesis of a serine elastase in arterial smooth muscle cells from multi-organ donors

Dominique Jourdheuil-Rahmania,*, Pierre H. Rollanda, Eugenio Rossetb, Alain Branchereaub and Danielle Garçona

aINSERM CJF 9401, Laboratory of Biochemistry, School of Pharmacy, Marseilles, France
bVascular Surgery Department, Sainte Marguerite Hospital, Marseilles, France

* Corresponding author. Laboratoire de Biochimie, Faculté de Pharmacie, 27 bld Jean Moulin, 13385 Marseille cedex 05, France. Tel.: +33 9183 5672; fax: +33 9125 4720.

Objectives: In heart transplant recipients with diffuse coronary arteriopathy, we have previously demonstrated the prevalence of elevated homocysteinemia, also known as an independent risk factor for myocardial infarction and stroke. In hyperhomocysteinemic mini-pigs we also observed early detectable pathologic changes in the elastic laminae. We hypothesized that homocysteine causes premature breakdown in the arterial elastic fibers by activation of the elastolytic activities. Methods: We examined the effect of homocysteine on elastase-like production by smooth muscle cells from sub-inguinal arteries of multi-organ donors (23.4±3.4 yr, n=8). The freshly isolated cells were incubated for 0–72 h with homocysteine (0–250 µM), in the presence or absence of specific protease inhibitors. Results: Homocysteine was devoid of a direct effect, but after 18 h incubation the elastase-like activities increased by 5–6-fold in the extracellular medium. The enzymes were characterized as serine proteases. Incubation of cells with a nucleic acid synthesis inhibitor (actinomycin D) or a protein synthesis inhibitor (cycloheximide) suppressed the enzyme induction. Conclusions: This is the first report of serine protease induction by homocysteine in vascular smooth muscle cells. The process may require protein synthesis and account for the early alterations of the arterial elastic structures in heart transplant recipients, and in other hyperhomocysteinemic patients, as well.

KEYWORDS Hcys = homocysteine; VSMC = vascular smooth muscle cells; SANA = N-succinyl trialanylnitroanilide; NMSN = N-methoxysuccinyl-Ala–Ala–Pro–Val-nitroanilide


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