Clinical and Experimental Obstetrics & Gynecology (CEOG) is published by IMR Press from Volume 47 Issue 1 (2020). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with S.O.G.
Progesterone receptor expression by human leukocyte celllines: molecular mechanisms of cytokine suppression
Purpose: We investigated progesterone (P) signaling in human leukemia cells, shown to downregulate cytokines with P. Methods: The following tests were utilized: PCR with FAM labeled primers and Gene Scan with the Applied Biosystems 373 DNA sequencer for progesterone receptor (PR) mRNA, immunohistochemistry using monoclonal antibodies (Zymed and Ventana) for PR protein, RT-PCR for glucocorticoid receptor (GR), NF kappa B (p65, p50, p52), c-rel, I kappa B-alpha, c-jun, c-fos, mRNA, transient transfections with pNF-kappa B-SEAP, and pGRE-SEAP vectors with chemiluminescence detection for NF kappa B and GR activity. Results: PR transcripts were demonstrated in MOT, U937, K562, THP-1, 8226, U226, not in JUKAT, HL60, HUT102, isolated normal peripheral blood mononuclear cells, or purified CD4+ or CD8+ T cells. Estradiol increased PR mRNA in MOT and U937. MOT, U937, K562, KG-1, 8226, ATL, and CD8+HTLV-1 expressed PR protein. SRIH-BATL, 729PH6NEO, HS-1, R-CLL, and JURKAT were negative. Steady state mRNA for GR, NF kappa B (p65, p50, p52), I kappa B-alpha, c-jun were unchanged with P in MOT and U937; c-fos and c-rel were not detected. There was a concentration-dependent reduction of NF kappa B activity with P in MOT and U937. Conclusion: The mechanism of cytokine suppression by P is mediated at least in part by suppression of NF kappa B, but the interaction of sex hormones, receptors, and transcription factors is complex.