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Submitted on August 23, 2005
Accepted on December 13, 2005
MRC Human Reproductive Science Unit (OPMS, SB, KJS and HNJ) and Department of Reproductive and Developmental Sciences (OPMS and HODC), The University of Edinburgh, Centre for Reproductive Biology, Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, United Kingdom
* To whom correspondence should be addressed. E-mail: h.jabbour{at}hrsu.mrc.ac.uk.
Prostacyclin (PGI) is a member of the prostanoid family of lipid mediators that mediates its effects through a seven-transmembrane G protein-coupled receptor (IP receptor). Recent studies have ascertained a role for prostanoid-receptor signaling in angiogenesis. In this study we examined the temporal-spatial expression of the IP receptor within normal human endometrium and additionally explored the signaling pathways mediating the role of IP receptor in activation of target angiogenic genes. Quantitative RT-PCR analysis demonstrated highest endometrial expression of the IP receptor in the menstrual phase, compared with all other stages of the menstrual cycle. Immunohistochemical analysis localized the site of IP receptor expression to the glandular epithelial compartment with stromal and perivascular cell immunoreactivity. Expression of immunoreactive IP receptor protein was greatest during the proliferative and early secretory phases of the menstrual cycle. To explore the role of the IP receptor in glandular epithelial cells, we used the Ishikawa endometrial epithelial cell line. Stimulation of Ishikawa cells and human endometrial biopsy explants with 100 nM Iloprost (a PGI analog) rapidly activated ERK1/2 signaling and induced the expression of the pro-angiogenic genes; basic fibroblast growth factor, angiopoetin-1 and angiopoetin-2 in an epidermal growth factor receptor (EGFR)-dependent manner. Furthermore, EGFR co-localized with IP receptor in the glandular epithelial compartment. These data suggest that PGI-IP interaction within glandular epithelial cells can promote the expression of pro-angiogenic genes in human endometrium via cross talk with the EGFR.
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