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Research Communications |
Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
Depletion of growth factors and glucocorticoids are known to induce apoptosis and inhibit growth in T lymphocytes. We have examined the effect of Bcl-2 expression on the cellular response to growth factor depletion in the presence or absence of glucocorticoids. Cell growth was determined by cell counting and viability was quantitated by dye exclusion. Apoptosis was evaluated by flow cytometry, analysis of DNA integrity, and enzymatic determination of caspase-3-like activity. Serum depletion and glucocorticoid administration inhibited cell growth and stimulated apoptosis in Bcl-2 negative cells. Cotreatment with both stimuli had additive effects on apoptosis but not on inhibition of cell growth. Bcl-2 expression abrogated the repressive effect of glucocorticoids on apoptosis but not on cell growth. In contrast, neither apoptosis nor growth inhibition induced by serum depletion of cells was blocked by Bcl-2 expression. However, glucocorticoid treatment of Bcl-2-overexpressing cells protected them from apoptosis induced by serum depletion. Glucocorticoid protection of Bcl-2-overexpressing cells from serum depletion-induced apoptosis was mimicked by other inducers of apoptosis, which act to inhibit protein synthesis. These data suggest that Bcl-2 expression can switch the effect of glucocorticoids from proapoptotic to antiapoptotic when lymphocytes expressing Bcl-2 are exposed to other apoptotic stimuli.—Huang, S.-T. J., Cidlowski, J. A. Glucocorticoids inhibit serum depletion-induced apoptosis in T lymphocytes expressing Bcl-2.
2 Correspondence: NIEHS, P.O. Box 12233, MD E2-02, Research Triangle Park, NC 27709, USA. E-mail: cidlowski{at}niehs.nih.gov
1 S.-T.J.H. is also a Ph.D. student of the Department of Cell and Molecular Physiology at the University of North Carolina at Chapel Hill, NC 27599, USA.
Key Words: programmed cell death • protection • growth factors
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