CLC number: R54; R34
On-line Access: 2024-08-27
Received: 2023-10-17
Revision Accepted: 2024-05-08
Crosschecked: 2013-06-18
Cited: 4
Clicked: 5634
Ya-fei Shi, Ju-fang Chi, Wei-liang Tang, Fu-kang Xu, Long-bin Liu, Zheng Ji, Hai-tao Lv, Hang-yuan Guo. Effects of rosuvastatin on the production and activation of matrix metalloproteinase-2 and migration of cultured rat vascular smooth muscle cells induced by homocysteine[J]. Journal of Zhejiang University Science B, 2013, 14(8): 696-704.
@article{title="Effects of rosuvastatin on the production and activation of matrix metalloproteinase-2 and migration of cultured rat vascular smooth muscle cells induced by homocysteine",
author="Ya-fei Shi, Ju-fang Chi, Wei-liang Tang, Fu-kang Xu, Long-bin Liu, Zheng Ji, Hai-tao Lv, Hang-yuan Guo",
journal="Journal of Zhejiang University Science B",
volume="14",
number="8",
pages="696-704",
year="2013",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.BQICC703"
}
%0 Journal Article
%T Effects of rosuvastatin on the production and activation of matrix metalloproteinase-2 and migration of cultured rat vascular smooth muscle cells induced by homocysteine
%A Ya-fei Shi
%A Ju-fang Chi
%A Wei-liang Tang
%A Fu-kang Xu
%A Long-bin Liu
%A Zheng Ji
%A Hai-tao Lv
%A Hang-yuan Guo
%J Journal of Zhejiang University SCIENCE B
%V 14
%N 8
%P 696-704
%@ 1673-1581
%D 2013
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.BQICC703
TY - JOUR
T1 - Effects of rosuvastatin on the production and activation of matrix metalloproteinase-2 and migration of cultured rat vascular smooth muscle cells induced by homocysteine
A1 - Ya-fei Shi
A1 - Ju-fang Chi
A1 - Wei-liang Tang
A1 - Fu-kang Xu
A1 - Long-bin Liu
A1 - Zheng Ji
A1 - Hai-tao Lv
A1 - Hang-yuan Guo
J0 - Journal of Zhejiang University Science B
VL - 14
IS - 8
SP - 696
EP - 704
%@ 1673-1581
Y1 - 2013
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.BQICC703
Abstract: Objective: To test the influence of homocysteine on the production and activation of matrix metalloproteinase-2 (MMP-2) and tissue inhibitors of matrix metalloproteinase-2 (TIMP-2) and on cell migration of cultured rat vascular smooth muscle cells (VSMCs). Also, to explore whether rosuvastatin can alter the abnormal secretion and activation of MMP-2 and TIMP-2 and migration of VSMCs induced by homocysteine. Methods: Rat VSMCs were incubated with different concentrations of homocysteine (50–5000 μmol/L). Western blotting and gelatin zymography were used to investigate the expressions and activities of MMP-2 and TIMP-2 in VSMCs in culture medium when induced with homocysteine for 24, 48, and 72 h. Transwell chambers were employed to test the migratory ability of VSMCs when incubated with homocysteine for 48 h. Different concentrations of rosuvastatin (10−9–10−5 mol/L) were added when VSMCs were induced with 1000 μmol/L homocysteine. The expressions and activities of MMP-2 and TIMP-2 were examined after incubating for 24, 48, and 72 h, and the migration of VSMCs was also examined after incubating for 48 h. Results: homocysteine (50–1000 μmol/L) increased the production and activation of MMP-2 and expression of TIMP-2 in a dose-dependent manner. However, when incubated with 5000 μmol/L homocysteine, the expression of MMP-2 was up-regulated, but its activity was down-regulated. Increased homocysteine-induced production and activation of MMP-2 were reduced by rosuvastatin in a dose-dependent manner whereas secretion of TIMP-2 was not significantly altered by rosuvastatin. homocysteine (50–5000 μmol/L) stimulated the migration of VSMCs in a dose-dependent manner, but this effect was eliminated by rosuvastatin. Conclusions: homocysteine (50–1000 μmol/L) significantly increased the production and activation of MMP-2, the expression of TIMP-2, and the migration of VSMCs in a dose-dependent manner. Additional extracellular rosuvastatin can decrease the excessive expression and activation of MMP-2 and abnormal migration of VSMCs induced by homocysteine.
[1]Arnaboldi, L., Guzzetta, M., Pazzucconi, F., Radaelli, G., Paoletti, R., Sirtori, C.R., Corsini, A., 2007. Serum from hypercholesterolemic patients treated with atorvastatin or simvastatin inhibits cultured human smooth muscle cell proliferation. Pharmacol. Res., 56(6):503-508.
[2]Bescond, A., Augier, T., Chareyre, C., Garçon, D., Hornebeck, W., Charpiot, P., 1999. Influence of homocysteine on matrix metalloproteinase-2: activation and activity. Biochem. Biophys. Res. Commun., 263(2):498-503.
[3]Busti, C., Falcinelli, E., Momi, S., Gresele, P., 2010. Matrix metalloproteinases and peripheral arterial disease. Intern. Emerg. Med., 5(1):13-25.
[4]Castro, R., Rivera, I., Blom, H.J., Jakobs, C., Tavares, de Almeida, I., 2006. Homocysteine metabolism, hyperhomocysteinaemia and vascular disease: an overview. J. Inherit. Metab. Dis., 29(1):3-20.
[5]Cheng-Lai, A., 2003. Rosuvastatin: a new HMG-CoA reductase inhibitor for the treatment of hypercholesterolemia. Heart Dis., 5(1):72-78.
[6]Guo, H., Lee, J.D., Ueda, T., Shan, J., Wang, J., 2003. Plasma homocysteine levels in patients with early coronary artery stenosis and high risk factors. Jpn. Heart J., 44(6):865-871.
[7]Guo, H., Lee, J.D., Uzui, H., Yue, H., Wang, P., Toyoda, K., Geshi, T., Ueda, T., 2007. Effects of heparin on the production of homocysteine-induced extracellular matrix metalloproteinase-2 in cultured rat vascular smooth muscle cells. Can. J. Cardiol., 23(4):275-280.
[8]Guo, H., Liu, L., Shi, Y., Sun, A., Xu, F., Chi, J., Huang, D., 2010. Chinese yellow wine and red wine inhibit matrix metalloproteinase-2 and improve atherosclerotic plaque in LDL receptor knockout mice. Cardiovasc. Ther., 28(3):161-168.
[9]Hagar, H.H., 2002. Folic acid and vitamin B12 supplementation attenuates isoprenaline-induced myocardial infarction in experimental hyperhomocysteinemic rats. Pharmacol. Res., 46(3):213-219.
[10]Holven, K.B., Aukrust, P., Holm, T., Ose, L., Nenseter, M.S., 2002. Folic acid treatment reduces chemokine release from peripheral blood mononuclear cells in hyperhomocysteinemic subjects. Arterioscler. Thromb. Vasc. Biol., 22(4):699-703.
[11]Kuzuya, M., Kanda, S., Sasaki, T., Tamaya-Mori, N., Cheng, X.W., Itoh, T., Itohara, S., Iguchi, A., 2003. Deficiency of gelatinase a suppresses smooth muscle cell invasion and development of experimental intimal hyperplasia. Circulation, 108(11):1375-1381.
[12]Li, D., Chen, H., Romeo, F., Sawamura, T., Saldeen, T., Mehta, J.L., 2002. Statins modulate oxidized low-density lipoprotein-mediated adhesion molecule expression in human coronary artery endothelial cells: role of LOX-1. J. Pharmacol. Exp. Ther., 302(2):601-605.
[13]Libby, P., Okamoto, Y., Rocha, V.Z., Folco, E., 2010. Inflammation in atherosclerosis: transition from theory to practice. Circ. J., 74(2):213-220.
[14]Löffek, S., Schilling, O., Franzke, C.W., 2011. Series “matrix metalloproteinases in lung health and disease”: Biological role of matrix metalloproteinases: a critical balance. Eur. Respir. J., 38(1):191-208.
[15]Luan, Z., Chase, A.J., Newby, A.C., 2003. Statins inhibit secretion of metalloproteinases-1, -2, -3, and -9 from vascular smooth muscle cells and macrophages. Arterioscler. Thromb. Vasc. Biol., 23(5):769-775.
[16]Moshal, K.S., Sen, U., Tyagi, N., Henderson, B., Steed, M., Ovechkin, A.V., Tyagi, S.C., 2006. Regulation of homocysteine-induced MMP-9 by ERK1/2 pathway. Am. J. Physiol. Cell Physiol., 290(3):C883-C891.
[17]Newby, A.C., 2005. Dual role of matrix metalloproteinases (matrixins) in intimal thickening and atherosclerotic plaque rupture. Physiol. Rev., 85(1):1-31.
[18]Puccetti, L., Acampa, M., Auteri, A., 2007. Pharmacogenetics of statins therapy. Recent Pat. Cardiovasc. Drug Discov., 2(3):228-236.
[19]Raffetto, J.D., Khalil, R.A., 2008. Matrix metalloproteinases and their inhibitors in vascular remodeling and vascular disease. Biochem. Pharmacol., 75(2):346-359.
[20]Steed, M.M., Tyagi, S.C., 2011. Mechanisms of cardiovascular remodeling in hyperhomocysteinemia. Antioxid. Redox Signal., 15(7):1927-1943.
[21]Uzui, H., Lee, J.D., Shimizu, H., Tsutani, H., Ueda, T., 2000. The role of protein-tyrosine phosphorylation and gelatinase production in the migration and proliferation of smooth muscle cells. Atherosclerosis, 149(1):51-59.
[22]Verreth, W., de Keyzer, D., Davey, P.C., Geeraert, B., Mertens, A., Herregods, M.C., Smith, G., Desjardins, F., Balligand, J.L., Holvoet, P., 2007. Rosuvastatin restores superoxide dismutase expression and inhibits accumulation of oxidized LDL in the aortic arch of obese dyslipidemic mice. Br. J. Pharmacol., 151(3):347-355.
[23]Ward, S., Lloyd Jones, M., Pandor, A., Holmes, M., Ara, R., Ryan, A., Yeo, W., Payne, N., 2007. A systematic review and economic evaluation of statins for the prevention of coronary events. Health Technol. Assess, 11(14):1-160, iii-iv.
[24]Weber, C., Noels, H., 2011. Atherosclerosis: current pathogenesis and therapeutic options. Nat. Med., 17(11):1410-1422.
[25]Zhou, J., Austin, R.C., 2009. Contributions of hyperhomocysteinemia to atherosclerosis: causal relationship and potential mechanisms. Biofactors, 35(2):120-129.
Open peer comments: Debate/Discuss/Question/Opinion
<1>