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Estrogen does not regulate CD154 mRNA stability in systemic lupus erythematosus T cellsDepartment of Biology, Pittsburg State University, Pittsburg, Kansas, USA, Department of Dermatology and Rheumatology, Kunming Medical College, Kunming, Peoples Republic of China
Department of Biology, Pittsburg State University, Pittsburg, Kansas, USA, vrider{at}pittstate.edu
Department of Radiation Oncology, The University of Kansas Medical Center, Kansas City, Kansas, USA
Center of Rheumatic Diseases, Allergy-Immunology, Kansas City, MO, USA
Previous studies in our laboratory showed a dose-dependent and hormone-specific increase in CD154 expression in T cells from females with systemic lupus erythematosus (SLE). This present study investigates if the estrogen-dependent increase in CD154 expression is due to stabilization of the messenger RNA. T cells from female SLE patients and controls were cultured for 18 h in serum-free medium without and with estradiol 17-ß (107 M). T cells were either unstimulated (resting) or were activated by further culture on anti-CD3 coated plates. Actinomycin D (25
Key Words: CD154 estrogen mRNA stability SLE T cell
Lupus, Vol. 15, No. 12,
852-857 (2006) This article has been cited by other articles:
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g/mL) was added to parallel cultures to inhibit new messenger RNA synthesis. CD154 messenger RNA stability was assessed by reverse-transcription polymerase chain amplification. Resting SLE (n = 10, P = 0.88) and normal (n = 7, P = 0.65) T cells showed no significant differences in message stability in response to estradiol. CD154 messenger RNA was also not significantly stabilized in activated SLE (n = 10, P = 0.15) or activated normal (n = 6, P = 0.077) T cells in response to estradiol. These findings indicate that the estrogen-dependent increase in CD154 in SLE T cells is not due to stability of the mRNA. These data are consistent with the postulate that estradiol stimulates CD154 transcription in SLE T cells. 