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[Cancer Research 43, 2536-2540, June 1, 1983]
© 1983 American Association for Cancer Research

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Glucocorticoid Effects on Lipopolysaccharide-stimulated Murine B-Cell Leukemia Line (BCL1) Cells1

Deborah A. Roess, Thomas S. Ruh, Clifford J. Bellone and Mary F. Ruh2

Departments of Physiology and Microbiology, St. Louis University, School of Medicine, St. Louis, Missouri 63104

The effects of glucocorticoids were studied in lipopolysaccharide (LPS)-stimulated splenic murine B-cell leukemia line one (BCL1) cells. At 24 hr, LPS caused a 3-fold increase in [3H]-thymidine incorporation compared to similarly cultured unstimulated cells. Triamcinolone acetonide (TA) and dexamethasone at a concentration of 10-8 M reduced [3H]thymidine incorporation 80 and 53%, respectively, while estradiol at concentrations of 10-10 to 10-5 M had no effect. A 500-fold excess of cortexolone or progesterone blocked the response of 10-8 M TA by 42 and 38%, respectively, indicating that the glucocorticoid response could be inhibited by antiglucocorticoids. The maximum rate of thymidine incorporation in LPS-stimulated cells occurred at 24 hr, a time at which 10-5 M TA present in parallel cultures from the initiation of LPS stimulation showed a 79% reduction in [3H]thymidine incorporation. If TA was added at any time after the initiation of LPS stimulation, the degree of decrease in nucleotide incorporation was not as marked. Therefore, maximum TA effect in LPS-stimulated BCL1 cells occurred when TA was added to cultures at the onset of mitogen stimulation. We also measured glucocorticoid-specific receptor in whole cells both before LPS stimulation and in BCL1 cells incubated 24 hr in the presence of LPS. The equilibrium dissociation constant, the number of sites/cell, and the hormone specificity of the glucocorticoid receptor were similar prior to and at the peak of mitogen stimulation.

1 This work was supported by Grant 24034, awarded by the National Cancer Institute, the Biomedical Research Support Grant of the USPHS to the St. Louis University School of Medicine, and the McBride-Love Foundation.

2 To whom requests for reprints should be addressed, at Department of Physiology, 1402 South Grand Boulevard, St. Louis, Mo. 63104.

Received 9/21/82. Accepted 3/ 3/83.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1983 by the American Association for Cancer Research.