Glucocorticoid regulation of cyclin D3 gene transcription and mRNA stability in lymphoid cells

Molecular Endocrinology
D Reisman, E A Thompson

Abstract

Glucocorticoids cause G0/G1 arrest of lymphoid cells. This is due, at least in part, to a decrease in the abundance of the G1 progression factor, cyclin D3. The mRNA encoding cyclin D3 (CcnD3 mRNA) is rapidly down-regulated when dexamethasone is added to P1798 murine T lymphoma cells. Fifty percent maximum inhibition is observed within about 2 h. Maximum inhibition of 75-85% obtains within 4-5 h. Cyclin D3 protein has a half-life of about 0.5 h in P1798 cells. Consequently, the abundance of cyclin D3 protein decreases in parallel with the abundance of CcnD3 mRNA. The effects of glucocorticoids are reversible. CcnD3 mRNA returns to near control levels within 2-3 h after removal of dexamethasone. Cyclin D3 protein recovers somewhat more slowly. The data indicate that glucocorticoids regulate the abundance of cyclin D3 mRNA. There is no significant decrease in nuclear run-on transcription of CcnD3 within 6 h after addition of glucocorticoids, although transcription is inhibited more than 80% after 24 h in the presence of dexamethasone. CcnD3 mRNA is very stable in mid-log phase P1798 cells, with a half-life of more than 8 h. The half-life of CcnD3 mRNA in glucocorticoid-treated cells is less than 1 h. Actinomycin D blocks the effe...Continue Reading

Citations

Jun 9, 2000·Journal of Neuroendocrinology·H TamuraI Wakabayashi
Mar 20, 2001·Gene·J Guhaniyogi, G Brewer
May 1, 2007·Biochemical and Biophysical Research Communications·Jianhai JiangJianxin Gu
Jun 1, 2002·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Christophe CrochemoreOsborne F X Almeida

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