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The Altered Distribution of the Steroid Hormone Receptors and the Chaperone Immunophilin FKBP52 in a Baboon Model of Endometriosis Is Associated With Progesterone Resistance During the Window of Uterine Receptivity
Kevin S. Jackson, PhD
Department of Obstetrics and Gynecology (MC808), College of Medicine, University of Illinois at Chicago
Allison Brudney
Department of Obstetrics and Gynecology (MC808), College of Medicine, University of Illinois at Chicago
Julie M. Hastings
Department of Obstetrics and Gynecology (MC808), College of Medicine, University of Illinois at Chicago
Patricia A. Mavrogianis
Department of Obstetrics and Gynecology (MC808), College of Medicine, University of Illinois at Chicago
J. Julie Kim
Department of Obstetrics and Gynecology, Division of Reproductive Biology, Northwestern University, Chicago, Illinois
Asgerally T. Fazleabas
Department of Obstetrics and Gynecology (MC808), College of Medicine, University of Illinois at Chicago, asgi{at}uic.edu
This study examines the distribution of estrogen receptors (ESR), progesterone receptors (Pgr), and the chaperone immunophilin FKBP52 in the eutopic endometrium in a baboon model of endometriosis during the window of receptivity to determine if their aberrant distribution contributes to reduced fecundity. Endometriosis was induced by inoculation of menstrual endometrium into the peritoneal cavity. Eutopic endometrium was collected at 3, 6, 9, 12, and 15 months postinoculation. Western blot (WB) and immunohistochemical analyses were performed. Isolated endometrial stromal cells were cultured in the presence or absence of steroid hormones. In animals with endometriosis, ESR-1 (ER- ) decreased in endometrial stromal cells, while ESR-2 (ER-ß) was reduced in both glandular epithelial (GE) and stromal cells. Immunoreactive total Pgr was markedly diminished in the GE, which was confirmed by WB analysis. Furthermore, treatment of isolated stromal cells from baboons with endometriosis with hormones did not increase levels of PRA or PRB as in control baboons. FKBP52 was also reduced in the eutopic endometrium of baboons with endometriosis. Endometriosis results in an aberrant distribution of ESR-1, ESR-2, Pgr, and FKBP52 in the eutopic endometrium. The authors propose that a dysregulation in the paracrine signaling between the endometrial stromal and GE cells reduces the responsiveness of Pgr, creating an endometrial environment that is unsuitable for implantation.
Key Words: KEY WORDS: Endometriosis • steroid receptors,immunohistochemistry • baboon • endometrial receptivity • uterus.
Reproductive Sciences, Vol. 14, No. 2,
137-150 (2007)
DOI: 10.1177/1933719106298409
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