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(The FASEB Journal. 1999;13:485-494.)
© 1999 FASEB

Research Communications

Bcl-2 alters the balance between apoptosis and necrosis, but does not prevent cell death induced by oxidized low density lipoproteins

OLIVIER MEILHAC, ISABELLE ESCARGUEIL-BLANC, JEAN-CLAUDE THIERS, ROBERT SALVAYRE 1 and ANNE NÈGRE-SALVAYRE 1

INSERM U-466 and Department of Biochemistry and Molecular Biology, IFR-31, CHU Rangueil, Toulouse, France

Oxidized low density lipoproteins (oxLDL) participate in atherosclerosis plaque formation, rupture, and subsequent thrombosis. Because oxLDL are toxic to cultured cells and Bcl-2 protein prevents apoptosis, the present work aimed to study whether Bcl-2 may counterbalance the toxicity of oxLDL. Two experimental model systems were used in which Bcl-2 levels were modulated: 1) lymphocytes in which the (high) basal level of Bcl-2 was reduced by antisense oligonucleotides; 2) HL60 and HL60/B (transduced by Bcl-2) expressing low and high Bcl-2 levels, respectively. In cells expressing relatively high Bcl-2 levels (lymphocytes and HL60/B), oxLDL induced mainly primary necrosis. In cells expressing low Bcl-2 levels (antisense-treated lymphocytes, HL60 and ECV-304 endothelial cells), the rate of oxLDL-induced apoptosis was higher than that of primary necrosis. OxLDL evoked a sustained calcium rise, which is a common trigger to necrosis and apoptosis since both types of cell death were blocked by the calcium chelator EGTA. Conversely, a sustained calcium influx elicited by the calcium ionophore A23187 induced necrosis in cells expressing high Bcl-2 levels and apoptosis in cells expressing low Bcl-2 levels. This suggests that Bcl-2 acts downstream from the calcium peak and inhibits only the apoptotic pathway, not the necrosis pathway, thus explaining the apparent shift from oxLDL-induced apoptosis toward necrosis when Bcl-2 is overexpressed.—Meilhac, O., Escargueil-Blanc, I., Thiers, J.-C., Salvayre, R., Nègre-Salvayre, A. Bcl-2 alters the balance between apoptosis and necrosis, but does not prevent cell death induced by oxidized low density lipoproteins.

1 Correspondence: Laboratoire de Biochimie, INSERM U-466, CHU Rangueil, 1 Ave. Jean Poulhès, 31403 Toulouse Cedex 4, France. E-mail: salvayre{at}rangueil.inserm.fr


Key Words: oxidized LDL • atherosclerosis • DNA ladder • cytosolic calcium concentration • antisense oligonucleotides




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