Heparin-binding epidermal growth factor and its receptors mediate decidualization and potentiate survival of human endometrial stromal cells

Chobotova, K. and Karpovich, N. and Carver, J. and Manek, S. and Gullick, W.J. and Barlow, D.H. and Mardon, H.J. (2005) Heparin-binding epidermal growth factor and its receptors mediate decidualization and potentiate survival of human endometrial stromal cells. Journal of Clinical Endocrinology and Metabolism, 90 (2). pp. 913-919. ISSN 0021-972X . (Access to this publication is restricted)

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http://dx.doi.org/10.1210/jc.2004-0476

Abstract

Heparin-binding epidermal growth factor (HB-EGF) has pleiotropic biological functions in many tissues, including those of the female reproductive tract. It facilitates embryo development and mediates implantation and is thought to have a function in endometrial receptivity and maturation. The mature HB-EGF molecule manifests its activity as either a soluble factor (sol-HB-EGF) or a transmembrane precursor (tm-HB-EGF) and can bind two receptors, EGFR and ErbB4/HER4. In this study, we identify factors that modulate expression of HB-EGF, EGFR, and ErbB4 in endometrial stromal cells in vitro. We demonstrate that levels of sol- and tm-HB-EGF, EGFR, and ErbB4 are increased by cAMP, a potent inducer of decidualization of the endometrial stroma. We also show that production of sol- and tm-HB-EGF is differentially modulated by TNF alpha and TGF beta. Our data suggest that HB-EGF has a function in endometrial maturation in mediating decidualization and attenuating TNF alpha- and TGF beta-induced apoptosis of endometrial stromal cells.

Item Type: Article
Uncontrolled keywords: Heparin-binding epidermal growth factor; ErbB4; Implantation
Subjects: Q Science
R Medicine > RC Internal medicine > RC0254 Neoplasms. Tumors. Oncology (including Cancer)
Divisions: Faculties > Science Technology and Medical Studies > School of Biosciences > Biomedical Research Group
Depositing User: Bill Gullick
Date Deposited: 01 Sep 2008 20:39
Last Modified: 05 Sep 2011 23:34
Resource URI: http://kar.kent.ac.uk/id/eprint/3975 (The current URI for this page, for reference purposes)
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