Am J Physiol Cell Physiol Journal of Applied Physiology
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Am J Physiol Cell Physiol 279: C1665-C1674, 2000;
0363-6143/00 $5.00
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Vol. 279, Issue 5, C1665-C1674, November 2000

beta -Adrenergic receptor/cAMP-mediated signaling and apoptosis of S49 lymphoma cells

Lizhen Yan, Volker Herrmann, Jason K. Hofer, and Paul A. Insel

Department of Pharmacology, University of California, San Diego, La Jolla, California 92093-0636

beta -Adrenergic receptor (beta AR) activation and/or increases in cAMP regulate growth and proliferation of a variety of cells and, in some cells, promote cell death. In the current studies we addressed the mechanism of this growth reduction by examining beta AR-mediated effects in the murine T-lymphoma cell line S49. Wild-type S49 cells, derived from immature thymocytes (CD4+/CD8+) undergo growth arrest and subsequent death when treated with agents that increase cAMP levels (e.g., beta AR agonists, 8-bromo-cAMP, cholera toxin, forskolin). Morphological and biochemical criteria indicate that this cell death is a result of apoptosis. In cyc- and kin- S49 cells, which lack Gsalpha and functional protein kinase A (PKA), respectively, beta AR activation of Gsalpha and cAMP action via PKA are critical steps in this apoptotic pathway. S49 cells that overexpress Bcl-2 are resistant to cAMP-induced apoptosis. We conclude that beta AR activation induces apoptosis in immature T lymphocytes via Gsalpha and PKA, while overexpression of Bcl-2 prevents cell death. beta AR/cAMP/PKA-mediated apoptosis may provide a means to control proliferation of immature T cells in vivo.

programmed cell death; protein kinase A; forskolin; Gsalpha


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