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Glycoxidation of low–density lipoprotein promotes multiple apoptotic pathways and NFkB activation in human coronary cells

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Abstract

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 LDL, but the biological effects of these modified lipoproteins are poorly understood. We demonstrate here that glycosylated oxLDL (glc–oxLDL) promotes apoptotic signaling in human coronary smooth muscle cells. This was associated by a decrease of the antiapoptotic protein Bcl–2, an increase of the pro–apoptotic protein Bax, and activation of caspase 3. Glc–oxLDL also activated NFkB and decreased IkB, these effects were more pronounced than those achieved with oxLDL. Our study shows that glc–oxLDL influences a broad cascade of signaling transduction pathways, which may not only result in apoptosis, but also could affect NFkB in human coronary cells. This cascade of events may influence the evolution of atherogenesis and vascular complications in diabetic patients.

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Correspondence to Claudio Napoli.

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de Nigris, F., Gallo, L., Sica, V. et al. Glycoxidation of low–density lipoprotein promotes multiple apoptotic pathways and NFkB activation in human coronary cells. Basic Res Cardiol 101, 101–108 (2006). https://doi.org/10.1007/s00395-005-0560-5

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  • DOI: https://doi.org/10.1007/s00395-005-0560-5

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