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Lupus
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Estrogen does not regulate CD154 mRNA stability in systemic lupus erythematosus T cells

X Li

Department of Biology, Pittsburg State University, Pittsburg, Kansas, USA, Department of Dermatology and Rheumatology, Kunming Medical College, Kunming, People’s Republic of China

V Rider

Department of Biology, Pittsburg State University, Pittsburg, Kansas, USA, vrider{at}pittstate.edu

B F Kimler

Department of Radiation Oncology, The University of Kansas Medical Center, Kansas City, Kansas, USA

N I Abdou

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 {sigma}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.

Key Words: CD154 • estrogen • mRNA stability • SLE • T cell

Lupus, Vol. 15, No. 12, 852-857 (2006)
DOI: 10.1177/0961203306071314


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