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Decidual Activin: Its Role In the Apoptotic Process and Its Regulation by Prolactin¹

Department of Physiology and Biophysics,⁷ University of Illinois, Chicago, Illinois 60612-7432 Department of Molecular and Cellular Physiology,⁸ University of Cincinnati, Cincinnati, Ohio 45267-0576

Successful pregnancy requires profound differentiation and reorganization of the uterine tissues including, as pregnancy progresses, extensive apoptosis of decidual tissue to accommodate the developing conceptus. We have previously shown a positive correlation between expression of activin A and apoptosis in the decidua and have also shown that expression of activin A occurs at the time when prolactin (PRL) receptors disappear from decidual cells. The goals of this study were to examine whether activin A plays a role in decidual apoptosis and whether expression of activin A in the decidua is regulated by PRL and placental lactogens. Studies were carried out using primary rat decidual cells, a decidual cell line (GG-AD), and PRL null mice. Treatment of decidual cells with activin A significantly increased DNA degradation, caspase 3 activity, and caspase 3 mRNA expression. However, this effect was observed only in the absence of endogenous activin production by these cells. Addition of follistatin to decidual cells that were producing activin A decreased both caspase 3 activity and mRNA expression. Similarly, addition of activin-blocking antibodies to cultures of GG-AD cells, which also produce activin A, caused a reduction in both DNA degradation and caspase 3 activity. PRL and placental lactogens caused an inhibition of activin A mRNA expression in primary decidual cells. Even more convincingly, decidua of PRL null mice expressed abundant activin A at a time when no expression of this hormone is detected in wild-type mice and treatment of PRL null mice with PRL caused a profound inhibition of activin A mRNA expression. In summary, our investigations into the role and regulation of decidual activin have revealed that activin A can induce cell death in the decidua and that its expression is under tight regulation by PRL and placental lactogens.

¹ This work was supported by National Institutes of Health grants HD-12356, U54 HD 40093, and HD-11119 (to G.G.), by the Ernst Schering Research Foundation (to C.T.), and by NIH grant T32 HL07692 (to J.M.B.-S.).

² Correspondence: Geula Gibori, Department of Physiology and Biophysics (M/C 901), University of Illinois, 835 S. Wolcott Avenue, Chicago, IL 60612-7342. FAX: 312 996 1414; ggibori{at}uic.edu

³ Current addresses: IUT Dijon, Bd Dr Petitjean BP 17867/UPRES Lipides et Nutrition, Universitè de Bourgogne, Facultè des Sciences de la Vie, 6 Bd Gabriel, 21000 Dijon, France

⁴ Current address: Laboratoire de Pharmacodynamie et Physiologie Pharmaceutique, Facultè de Pharmacie, BP 87900, 21079 Dijon Cedex, France

⁵ Current address: Division of Basic Biomedical Sciences, University of South Dakota School of Medicine, 414 East Clark Street, Vermillion, SD 57069

⁶ Current address: FDA/CFSAN, 5100 Paint Branch Pkwy, College Park, HFS-275, MD 20740

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