Glycoxidation of low-density lipoprotein increases TUNEL positivity and CPP32 activation in human coronary cells

被引:6
作者
De Nigris, F [1 ]
Tajana, G
Condorelli, M
D'Armiento, FP
Sica, G
Lerman, LO
Napoli, C
机构
[1] Univ Salerno, Fac Pharm, Dept Pharmacol Sci, Chair Anat, I-84084 Fisciano, Italy
[2] Univ Naples Federico II, Dept Med, Naples, Italy
[3] Univ Naples Federico II, Dept Human Pathol, Naples, Italy
[4] Univ Naples Federico II, Dept Clin Pathol, Naples, Italy
[5] Mayo Clin & Mayo Fdn, Dept Med, Div Hypertens, Rochester, MN 55905 USA
来源
APOPTOSIS: FROM SIGNALING PATHWAYS TO THERAPEUTIC TOOLS | 2003年 / 1010卷
关键词
atherosclerosis; glc-oxLDL; oxLDL; caspase;
D O I
10.1196/annals.1299.128
中图分类号
Q2 [细胞生物学];
学科分类号
071009 [细胞生物学]; 090102 [作物遗传育种];
摘要
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 (gle-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.
引用
收藏
页码:710 / 715
页数:6
相关论文
共 19 条
[1]
Oxidized LDL promotes peroxide-mediated mitochondrial dysfunction and cell death in human macrophages - A caspase-3-independent pathway [J].
Asmis, R ;
Begley, JG .
CIRCULATION RESEARCH, 2003, 92 (01) :E20-E29
[2]
Contrary effects of lightly and strongly oxidized LDL with potent promotion of growth versus-apoptosis on arterial smooth muscle cells, macrophages, and fibroblasts [J].
Bjorkerud, B ;
Bjorkerud, S .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1996, 16 (03) :416-424
[3]
Increase in TUNEL positive cells in aorta from diabetic rats [J].
Chu, Y ;
Faraci, FM ;
Ooboshi, H ;
Heistad, DD .
ENDOTHELIUM-NEW YORK, 1997, 5 (04) :241-250
[4]
Oxidation-sensitive mechanisms, vascular apoptosis and atherosclerosis [J].
de Nigris, F ;
Lerman, A ;
Ignarro, LJ ;
Williams-Ignarro, S ;
Sica, V ;
Baker, AH ;
Lerman, LO ;
Geng, YJ ;
Napoli, C .
TRENDS IN MOLECULAR MEDICINE, 2003, 9 (08) :351-359
[5]
Modulation by α- and γ-tocopherol and oxidized low-density lipoprotein of apoptotic signaling in human corollary smooth muscle cells [J].
de Nigris, F ;
Franconi, F ;
Maida, I ;
Palumbo, G ;
Anania, V ;
Napoli, C .
BIOCHEMICAL PHARMACOLOGY, 2000, 59 (11) :1477-1487
[6]
Oxidation-sensitive transcription factors and molecular mechanisms in the arterial wall [J].
De Nigris, F ;
Lerman, LO ;
Condorelli, M ;
Lerman, A ;
Napoli, C .
ANTIOXIDANTS & REDOX SIGNALING, 2001, 3 (06) :1119-1130
[7]
In vivo and in vitro evidence for the glycoxidation of low density lipoprotein in human atherosclerotic plaques [J].
Imanaga, Y ;
Sakata, N ;
Takebayashi, S ;
Matsunaga, A ;
Sasaki, J ;
Arakawa, K ;
Nagai, R ;
Horiuchi, S ;
Itabe, H ;
Takano, T .
ATHEROSCLEROSIS, 2000, 150 (02) :343-355
[8]
DNA fragmentation and ultrastructural changes of degenerating cells in atherosclerotic lesions and smooth muscle cells exposed to oxidized LDL in vitro [J].
Jovinge, S ;
Crisby, M ;
Thyberg, J ;
Nilsson, J .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1997, 17 (10) :2225-2231
[9]
KENNEDY L, 1984, DIABETOLOGIA, V26, P93
[10]
LOWRY OH, 1951, J BIOL CHEM, V193, P265