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Glycoxidation of Low-Density Lipoprotein Increases TUNEL Positivity and CPP32 Activation in Human Coronary Cells
aDepartment of Pharmacological Sciences, Chair of Anatomy, Faculty of Pharmacy, University of Salerno, Fisciano-Salerno, Italy bDepartments of Medicine and Human Pathology and Clinical Pathology, University of Naples, Naples, Italy dDepartment of Medicine, Division of Hypertension, Mayo Clinic, Rochester, Minnesota, USA
Address for correspondence: F. de Nigris, Ph.D., Department of Pharmacological Sciences, Chair of Anatomy, Faculty of Pharmacy, University of Salerno, 84084 Fisciano-Salerno, Italy. fnigris{at}yahoo.com Ann. N.Y. Acad. Sci. 1010: 710-715 (2003).
Apoptosis of arterial cells induced by oxidized low-density lipoprotein (oxLDL) is thought to contribute to the progression of vascular dysfunction and atherogenesis. It is well established that diabetes mellitus is accompanied by both glycosylation and oxidation of LDL (glc-oxLDL), but the biological effects of these modified lipoproteins are poorly understood. We demonstrate here for the first time that glc-oxLDL increases TUNEL positivity and caspase-3 activation (by Western blot and immunocytochemistry) of human coronary smooth muscle cells. Overall, these effects induced by glc-oxLDL were greater than those achieved with oxLDL. Thus, glc-oxLDL activated downstream apoptotic signaling. This may influence the evolution of atherogenesis and vascular complications in diabetes.
Key Words: atherosclerosis • glc-oxLDL • oxLDL • caspase This article has been cited by other articles:
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