HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 73/2/261    most recent biolreprod.105.041061v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal My Folders Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Peluso, J. J. Articles by Wehling, M. Search for Related Content PubMed PubMed Citation Articles by Peluso, J. J. Articles by Wehling, M. Agricola Articles by Peluso, J. J. Articles by Wehling, M.

Expression and Function of PAIRBP1 Within Gonadotropin-Primed Immature Rat Ovaries: PAIRBP1 Regulation of Granulosa and Luteal Cell Viability¹

Departments of Cell Biology² Obstetrics and Gynecology,³ University of Connecticut Health Center, Farmington, Connecticut 06030 Faculty of Clinical Medicine Mannheim,⁴ Institute of Clinical Pharmacology, University of Heidelberg, Mannheim, D-68167 Germany Medicine/Experimental Medicine,⁵ AstraZeneca R&D, S48183 Molndal, Sweden

The protein PAIRBP1, which was initially referred to as RDA288, is involved in mediating the antiapoptotic action of progesterone (P4) in spontaneously immortalized granulosa cells (SIGCs). The present studies were designed to assess the expression and function of PAIRBP1 in the different cell types within the immature rat ovary. Western blot analysis detected PAIRBP1 within whole-cell lysates of immature rat ovaries. Equine gonadotropin (eCG) induced a 3-fold increase in ovarian levels of PAIRBP1. Moreover, human chorionic gonadotropin (hCG), given 48 h after eCG, maintained these elevated levels for up to 4 days. Immunohistochemical analysis confirmed this and further demonstrated that interstitial, thecal, and surface epithelial cells also expressed PAIRBP1. The level of PAIRBP1 in these cells was not influenced by gonadotropin treatment. In contrast, eCG stimulated an increase in PAIRBP1 within the granulosa cells of the developing follicles. Treatment with hCG induced ovulation and ultimately the formation of corpora lutea (CL). High levels of PAIRBP1 expression were also observed within the luteal cells. Immunocytochemical studies on living, nonpermeabilized granulosa and luteal cells revealed that some PAIRBP1 localized to the extracellular surface of these cells. The presence of PAIRBP1 on the extracellular surface was consistent with the observation that an antibody to PAIRBP1 attenuated P4's antiapoptotic action in both granulosa and luteal cells. Although the PAIRBP1 antibody attenuated P4's action, it did not reduce the capacity of cells to specifically bind ³H-P4. Immunoprecipitation with the PAIRBP1 antibody pulled down the membrane P4 binding protein known as progesterone receptor membrane complex-1 (PGRMC1; rat homolog accession number AJ005837). Taken together, these findings suggest that gonadotropins regulate the expression of PAIRBP1 in granulosa and luteal cells and that PAIRBP1 plays an important role in mediating P4's antiapoptotic action in these ovarian cell types. The exact mechanism of PAIRBP1's action remains to be elucidated, but it may involve an interaction with PGRMC1.

apoptosis, corpus luteum, granulosa cells, luteal cell, progesterone, signal transduction

² Correspondences: Department of Cell Biology, University of Connecticut Health Center, Farmington, CT 06030. FAX: 860 6791269; peluso{at}nso2.uchc.edu

This article has been cited by other articles:

				P. A. Friberg, D.G. J. Larsson, and H. Billig Dominant Role of Nuclear Progesterone Receptor in the Control of Rat Periovulatory Granulosa Cell Apoptosis Biol Reprod, June 1, 2009; 80(6): 1160 - 1167. [Abstract] [Full Text] [PDF]

				B. Gellersen, M.S. Fernandes, and J.J. Brosens Non-genomic progesterone actions in female reproduction Hum. Reprod. Update, January 1, 2009; 15(1): 119 - 138. [Abstract] [Full Text] [PDF]

				J. J. Peluso, X. Liu, M. M. Saunders, K. P. Claffey, and K. Phoenix Regulation of Ovarian Cancer Cell Viability and Sensitivity to Cisplatin by Progesterone Receptor Membrane Component-1 J. Clin. Endocrinol. Metab., May 1, 2008; 93(5): 1592 - 1599. [Abstract] [Full Text] [PDF]

				J. J. Peluso, J. Romak, and X. Liu Progesterone Receptor Membrane Component-1 (PGRMC1) Is the Mediator of Progesterone's Antiapoptotic Action in Spontaneously Immortalized Granulosa Cells As Revealed by PGRMC1 Small Interfering Ribonucleic Acid Treatment and Functional Analysis of PGRMC1 Mutations Endocrinology, February 1, 2008; 149(2): 534 - 543. [Abstract] [Full Text] [PDF]

				P.-J. He, M. Hirata, N. Yamauchi, S. Hashimoto, and M.-a. Hattori The disruption of circadian clockwork in differentiating cells from rat reproductive tissues as identified by in vitro real-time monitoring system J. Endocrinol., June 1, 2007; 193(3): 413 - 420. [Abstract] [Full Text] [PDF]

				T. Krietsch, M. S. Fernandes, J. Kero, R. Losel, M. Heyens, E. W.-F. Lam, I. Huhtaniemi, J. J. Brosens, and B. Gellersen Human Homologs of the Putative G Protein-Coupled Membrane Progestin Receptors (mPR{alpha}, {beta}, and {gamma}) Localize to the Endoplasmic Reticulum and Are Not Activated by Progesterone Mol. Endocrinol., December 1, 2006; 20(12): 3146 - 3164. [Abstract] [Full Text] [PDF]

				L. Engmann, R. Losel, M. Wehling, and J. J. Peluso Progesterone Regulation of Human Granulosa/Luteal Cell Viability by an RU486-Independent Mechanism J. Clin. Endocrinol. Metab., December 1, 2006; 91(12): 4962 - 4968. [Abstract] [Full Text] [PDF]

				J. J. Peluso Multiplicity of Progesterone's Actions and Receptors in the Mammalian Ovary Biol Reprod, July 1, 2006; 75(1): 2 - 8. [Abstract] [Full Text] [PDF]

				J. J. Peluso, A. Pappalardo, R. Losel, and M. Wehling Progesterone Membrane Receptor Component 1 Expression in the Immature Rat Ovary and Its Role in Mediating Progesterone's Antiapoptotic Action Endocrinology, June 1, 2006; 147(6): 3133 - 3140. [Abstract] [Full Text] [PDF]