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. 2007 Feb;27(1):20-3.
doi: 10.1007/s11596-007-0106-1.

Influence of oxidized low density lipoprotein on the proliferation of human artery smooth muscle cells in vitro

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Influence of oxidized low density lipoprotein on the proliferation of human artery smooth muscle cells in vitro

Chenhui Qiao et al. J Huazhong Univ Sci Technolog Med Sci. 2007 Feb.

Retraction in

  • Editorial retraction.
    [No authors listed] [No authors listed] J Huazhong Univ Sci Technolog Med Sci. 2008 Apr;28(2):234. doi: 10.1007/s11596-008-0231-5. J Huazhong Univ Sci Technolog Med Sci. 2008. PMID: 18481007 No abstract available.

Abstract

The effects of oxidized low density lipoprotein (ox-LDL) on the proliferation of cultured human vascular smooth muscle cells (vSMC) were investigated in vitro. By using NaBr density gradient centrifugation, LDL was isolated and purified from human plasma. Ox-LDL was produced from LDL by being incubated with CuSO(4). ox-LDL was then added to the culture medium at different concentrations (35, 60, 85, 110, 135 and 160 microg/mL) for 7 days. The influence of ox-LDL on vSMC proliferation was observed in growth curve, mitosis index, and in situ determination of apoptosis. The data were analyzed with SPSS 10.0 software. The results showed that the ox-LDL produced in vitro had a good purity and optimal oxidative degree, which was similar to the intrinsic ox-LDL in atherosclerotic plaque. ox-LDL at a concentration of 35 microg/mL demonstrated the strongest proliferation inducement, and at a concentration of 135 microg/mL, ox-LDL could inhibit the growth of vSMC. ox-LDL at concentrations of 35 and 50 microg/mL presented powerful mitotic trigger, and with the increase of ox-LDL concentration, the mitotic index of vSMC was decreased gradually. ox-LDL at higher concentrations promoted more apoptotic vSMCs. ox-LDL at lower concentrations triggered proliferation of vSMCs, and at higher concentrations induced apoptosis in vSMCs. ox-LDL played a promotional role in the pathogenesis and development of atherosclerosis by affecting vSMC proliferation and apoptosis.

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