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. 2010 Apr;25(2):133-40.
doi: 10.1007/s12291-010-0025-y. Epub 2010 May 27.

Matrix metalloproteinase-3 (MMP-3) -1612 5A/6A promoter polymorphism in coronary artery disease in Indian population

Kavita K Shalia  1 , V K Shah, M R Mashru, S L Soneji, J B Vasvani, S Payannavar, A Walvalkar, R Mokal, S S Mithbawkar, M Bootwalla, P Sadvekar, P K Thakur
Affiliations

Matrix metalloproteinase-3 (MMP-3) -1612 5A/6A promoter polymorphism in coronary artery disease in Indian population

Kavita K Shalia et al. Indian J Clin Biochem. 2010 Apr.

Abstract

Matrix metalloproteinases (MMPs) play important role in the pathogenesis of coronary artery disease (CAD). 5A allele of -1612 5A/6A polymorphism of MMP-3 is associated with two fold higher activity than 6A allele. Present study was designed to analyse the association of this polymorphism with CAD in Indian population. Subjects included in the study were patients with stable angina (n=35), unstable angina (n=53), patients with recent event of myocardial infarction (MI) (MI Group-1, n=56) and patients at presentation of the acute MI (MI Group-2, n=49). Controls were healthy individuals (n=99). Genotyping of MMP-3 5A/6A polymorphism was carried out by PCR-based restriction digestion method. The genotype distribution of patient groups did not deviate from controls. Serum MMP-3 levels were significantly elevated at presentation of the acute MI by 36.8% (P=0.031) as compared to controls and more associated with 6A genotype suggesting discrepancy between in vitro transfection experiment and peripheral MMP-3 levels.

Keywords: Coronary artery disease; Matrix metalloproteinase-3; Myocardial infarction; Single nucleotide polymorphism; Stable angina; Unstable angina.

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References

    1. Mtairag E.M., Chollet-Martin S., Oudghiri M., Laquay N., Marie-Paule J., Jean-Baptiste, et al. Effects of interleukin-10 on monocyte/endothelial cell adhesion and MMP-9/TIMP-1 secretion. Cardiovasc Res. 2001;49:882–890. doi: 10.1016/S0008-6363(00)00287-X. - DOI - PubMed
    1. Ardans J.A., Blum A., Mangan P.R., Wientroub S., Cannon R.O., 3rd, Wahl L.M. Raloxifene-mediated increase in matrix metalloproteinase-1 production by activated monocytes. Arterioscler Thromb Vasc Biol. 2001;21:1265–1268. doi: 10.1161/hq0801.095083. - DOI - PubMed
    1. Ravn H.B., Falk E. Histopathology of plaque rupture. Cardiol Clin. 1999;17:263–270. doi: 10.1016/S0733-8651(05)70073-4. - DOI - PubMed
    1. Shah P.K., Falk E., Badimon J.J., Fernandez-Ortiz A., Mailhac A., Villareal-Levy G., et al. Human monocyte-derived macrophages induce collagen breakdown in fibrous caps of atherosclerotic plaques. Potential role of matrix-degrading metalloproteinases and implications for plaque rupture. Circulation. 1995;92:1565–1569. - PubMed
    1. Galis Z.S., Sukhova G.K., Lark M.W., Libby P. Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques. J Clin Invest. 1994;94:2493–2503. doi: 10.1172/JCI117619. - DOI - PMC - PubMed

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