Effect of glucocorticosteroid treatment on intracellular calcium homeostasis in mouse lymphoma cells. (original) (raw)
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1Ireland Cancer Center, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106-4937.
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1Ireland Cancer Center, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106-4937.
Search for other works by this author on:
1Ireland Cancer Center, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106-4937.
Search for other works by this author on:
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M Lam, G Dubyak, C W Distelhorst, Effect of glucocorticosteroid treatment on intracellular calcium homeostasis in mouse lymphoma cells., Molecular Endocrinology, Volume 7, Issue 5, 1 May 1993, Pages 686–693, https://doi.org/10.1210/mend.7.5.8316252
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Abstract
There is growing evidence for the involvement of Ca2+ in the programmed cell death (apoptosis) of lymphocytes, but the nature of glucocorticoid-induced Ca2+ fluxes and their role in the cell death pathway are poorly understood. In the study reported here, we assessed the effect of glucocorticoid treatment on intracellular Ca2+ homeostasis in W7MG1 mouse lymphoma cells. Levels of cytosolic Ca2+ were measured using the intracellular Ca2+ indicator fura2 AM, and total cellular Ca2+ was measured by atomic absorbance spectroscopy. The level of Ca2+ within internal stores, including the endoplasmic reticulum (ER), was estimated by measuring the increase in cytosolic Ca2+ induced by either ionomycin, an ionophore that mobilizes Ca2+ from a variety of internal stores, and by thapsigargin, a specific inhibitor of the ER-associated Ca(2+)-ATPase that mobilizes Ca2+ from the ER. Glucocorticoid treatment induced a significant decrease in ionomycin- and thapsigargin-mobilizable Ca2+ stores that was accompanied by an initial decrease in total cellular Ca2+, followed by a modest increase in both total cellular Ca2+ and cytosolic Ca2+. The glucocorticoid-induced depletion of internal Ca2+ stores was receptor mediated and occurred after a delay corresponding to the time required for glucocorticoid receptor complexes to regulate gene transcription. Mobilization of ER-associated Ca2+ stores by thapsigargin treatment induced DNA fragmentation and cell death similar to that observed after glucocorticoid treatment. These findings suggest that a mobilization of Ca2+ from internal stores may be a critical step in the apoptotic pathway of mouse lymphoma cells.
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Copyright © 1993 by The Endocrine Society
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