title: Reproductive hormones in the regulation of apoptosis of neutrophils.
abstract: The ability of main reproductive hormones such as chorionic gonadotropin (CG), estradiol, and progesterone to regulate apoptosis of human neutrophils was studied. The hormones were studied separately and in physiological combinations specific for different trimesters of pregnancy. A low dose of CG (10 IU/ml) increased the spontaneous apoptosis of neutrophils, whereas its combination with estradiol and progesterone corresponding to that of trimester III of pregnancy significantly decreased this parameter. The stimulating effect of CG was prevented by an inhibitor of protein kinase A, whereas the hormone-induced suppression of apoptosis depended on the activity of Ca2+-channels. The antiapoptotic effect of the hormonal combination corresponding to that of trimester III was also manifested in the presence of autologous T-lymphocytes and on stimulation of neutrophils by bacterial lipopolysaccharide. The apoptosis induced with monoclonal antibodies to CD95 was significantly suppressed by the hormones studied and their combinations. Thus, apoptosis of neutrophils is effectively regulated by reproductive hormones; this seems to be an important control mechanism of activation of these cells in pregnancy.
authors.affiliation: Institute of Ecology and Genetics of Microorganisms, Ural Division, Russian Academy of Sciences, ul. Goleva 13, Perm 614081, Russia. conf@ecology.psu.ru
authors.forename: S V
authors.initials: SV
authors.lastname: Shirshev
authors.forename: E M
authors.initials: EM
authors.lastname: Kuklina
authors.forename: A A
authors.initials: AA
authors.lastname: Yarilin
mesh_terms: D000067956:Adenylyl Cyclase Inhibitors; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects* / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D006063:Chorionic Gonadotropin / Q000494:pharmacology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D006885:Hydroxybutyrates / Q000494:pharmacology; D007546:Isoquinolines / Q000494:pharmacology; D009504:Neutrophils / Q000166:cytology* / Q000276:immunology / Q000378:metabolism; D009942:Organometallic Compounds / Q000494:pharmacology; D011247:Pregnancy; D011261:Pregnancy Trimester, First; D011263:Pregnancy Trimester, Third; D011374:Progesterone / Q000494:pharmacology*; D013449:Sulfonamides; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D014700:Verapamil / Q000494:pharmacology; D019014:fas Receptor / Q000276:immunology / Q000378:metabolism
chemical_list: D000067956:Adenylyl Cyclase Inhibitors; D000911:Antibodies, Monoclonal; D002121:Calcium Channel Blockers; D006063:Chorionic Gonadotropin; D004791:Enzyme Inhibitors; D006885:Hydroxybutyrates; D007546:Isoquinolines; D009942:Organometallic Compounds; D013449:Sulfonamides; D019014:fas Receptor; D011374:Progesterone; D004958:Estradiol; C022826:lithium hydroxybutyrate; D014700:Verapamil; C063509:N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide