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Am J Physiol Cell Physiol 281: C1596-C1603, 2001;
0363-6143/01 $5.00
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Vol. 281, Issue 5, C1596-C1603, November 2001

Hypoxia induces apoptosis via two independent pathways in Jurkat cells: differential regulation by glucose

Ricky Malhotra1, Zhiwu Lin1, Claudius Vincenz2, and Frank C. Brosius III1

Division of Nephrology, Departments of 1 Internal Medicine and 2 Pathology, University of Michigan Medical School and Ann Arbor Veterans Affairs Hospital, Ann Arbor, Michigan 48109

Glucose uptake and metabolism inhibit hypoxia-induced apoptosis in a variety of cell types, but the underlying molecular mechanisms remain poorly understood. In the present study, we explore hypoxia-mediated cell death pathways in Jurkat cells in the presence and absence of extracellular glucose. In the absence of extracellular glucose, hypoxia caused cytochrome c release, caspase 3 and poly(ADP-ribose)polymerase cleavage, and DNA fragmentation; this apoptotic response was blocked by the caspase 9 inhibitor z-LEHD-FMK. The presence of extracellular glucose during hypoxia prevented cytochrome c release and activation of caspase 9 but did not prevent apoptosis in Jurkat cells. In these conditions, overexpression of the caspase 8 inhibitor v-FLIP prevented hypoxia-mediated cell death. Thus hypoxia can stimulate two apoptotic pathways in Jurkat cells, one dependent on cytochrome c release from mitochondria that is prevented by glucose uptake and metabolism, and the other independent of cytochrome c release and resulting from activation of the death receptor pathway, which is accelerated by glucose uptake and metabolism.

cytochrome c; viral FLICE inhibitory protein; death receptor; caspases


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