Studies on the induction of apoptosis in WEHI 231 cells by pharmacological agents and lipid mediators. Sphingosine and ceramide induce apoptosis in WEHI 231

J Quintans; G A Bonn; C L McShan; A R Gottschalk

Studies on the induction of apoptosis in WEHI 231 cells by pharmacological agents and lipid mediators. Sphingosine and ceramide induce apoptosis in WEHI 231

Cell Death Differ. 1994;1(2):93-9.

Authors

J Quintans¹, G A Bonn, C L McShan, A R Gottschalk

Affiliation

¹ Department of Pathology and The Cancer Research Center, University of Chicago, Chicago, III. 60637 USA.

PMID: 17180022

Abstract

We report the results of a systematic study of the effects of pharmacological agents known to cause or modify physiological cell death (PCD). Using WEHI 231 cells as a model, we investigated the effects of dexamethasone, cAMP, selected growth factors/ cytokines, DNA damaging agents, metabolic inhibitors and lipid mediators. We found that WEHI 231 cells are not affected by cAMP(1-90 microM) or TGFbeta (1-50 ng/ml), both of which are known to induce PCD in other systems. We also failed to detect protection from PCD in WEHI 231 cells cultured with Zn(++), E64 and leupeptin. In contrast, dexamethasone (400 microg/ml), etoposide (10(-4)M), emetine (10(-5)M), calyculin (10(-5)M), sphingosine (8-16 microM) and ceramide (20-40 microM) all cause PCD in WEHI 231 cells. The effects of ceramide can be blocked by LPS but not by overexpression of bcl2.The role of killer lipids in PCD is discussed.