Fertility

New data from University of Connecticut illuminate research in hormones

"In vitro studies were conducted on GL cells from women undergoing in vitro fertilization and GL5 cells, which are derived from GL cells. GL cells were obtained from women undergoing fertility treatment at a university-based clinic and used for in vitro studies. PCR, Western blot, and immunocytochemistry were used to detect various progestin binding proteins. H-3-P4 binding kinetics were assessed on partially purified PGRMC1. Apoptosis was determined after culture by either TUNEL or DAPI staining. P4 was measured by an ELISA assay. PGRMC1 was depleted using small interfering RNA. GL and GL5 cells expressed several P4 binding proteins including the nuclear progesterone receptor (PGR), progestin/adipoQ receptors (PAQR7, 8, and 5) and PGRMC1. Ligand binding studies revealed that both P4 and the progestin, R5020, bound PGRMC1 with an EC50 of approximately 10 nM. Interestingly, P4 inhibited apoptosis at concentrations in the 10 nM range, whereas R5020 stimulated P4 secretion at concentrations of at lease 16 mc M. Depleting PGRMC1 attenuated P4's antiapoptotic action but failed to influence R5020-induced P4 secretion. These studies conclusively demonstrate that in human GL cells PGRMC1 functions as a receptor through which P4 activates a signal cascade that prevents apoptosis," wrote J.J. Peluso and colleagues, University of Connecticut.

The researchers concluded: "In contrast, PGRMC1 does not mediate P4's ability to acutely promote its own secretion. (J Clin Endocrinol Metab 94: 2644-2649, 2009)."

Peluso and colleagues published their study in the Journal of Clinical Endocrinology & Metabolism (Progesterone Activates a Progesterone Receptor Membrane Component 1-Dependent Mechanism That Promotes Human Granulosa/Luteal Cell Survival But Not Progesterone Secretion. Journal of Clinical Endocrinology & Metabolism, 2009;94(7):2644-2649).

For additional information, contact J.J. Peluso, University of Connecticut, Center Health, Dept. of Cell Biology, Farmington, CT 06030, USA.

The publisher of the Journal of Clinical Endocrinology & Metabolism can be contacted at: Endocrine Society, 8401 Connecticut Avenue, Suite 900, Chevy Chase, MD 20815-5817, USA.

Keywords: United States, Farmington, Apoptosis, Clinical Endocrinology, Drugs, Hormones, Metabolism, Pharmaceuticals, Progesterone, Therapy, Treatment, University of Connecticut.

This article was prepared by Biotech Business Week editors from staff and other reports. Copyright 2009, Biotech Business Week via NewsRx.com.