Examination of estradiol 17-b (E2) role in the regulation of corpus luteum function during pregnancy in rats: Involvement of IGFBP5 in the E2-mediated actions

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: MON 515-547-Female Reproductive Endocrinology
Basic/Translational
Monday, June 17, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board MON-522
Sudeshna Tripathy* and Medhamurthy Rudraiah
INDIAN INSTITUTE OF SCIENCE, BANGALORE, India
Corpus luteum (CL), a transient endocrine tissue formed post ovulation is essential for establishment and maintenance of pregnancy in mammals.  Although expression of Cyp19A1 gene gets down regulated post ovulation, but the expression rebounds and aromatase participates in the luteal biosynthesis of E2. Previous studies have suggested participation of intraluteal E2 in the regulation of CL function, steroidogenesis and cell proliferation. To further understand the E2 effects at the molecular level, aromatase inhibitor (AI), anastrozole was administered orally during early (day 7-11) and mid (day 12-15) pregnancy in rats. A decline in mRNA and protein levels of aromatase was observed during mid pregnancy. Additionally, replacement of exogenous E2 was carried out during AI treatment on day 12-15 of pregnancy. A significant decline was observed in serum estradiol (143.33±6.67 vs. 110.83±4.36 pg/ml), intraluteal estradiol levels (19.48±3.43 vs. 8.09±1.82 pg/mg CL tissue) and weight of CL (4.82±0.12 vs. 2.86±0.17 mg/CL) post AI treatment. The diminished weight of CL was recovered (2.86±0.17 vs. 4.5±0.29 mg/CL) by E2 replacement during AI treatment. Global gene expression profiling (GEO database, GSE41735) of CL tissues collected post treatments revealed a plethora of differentially expressed genes after AI treatment and 92 E2- responsive genes were identified with a view to identify various factors downstream of E2 signaling. Gene ontology further segregated many of the E2 -responsive growth factors into different biological processes. Significant up regulation of one of the IGFBPs, IGFBP5 along with PI3K p85 phosphorylation at protein levels led us to investigate the role of IGFBP5 in controlling luteal cell proliferation, survival or apoptosis. Preliminary histological staining revealed difference in luteal cell number after E2 withdrawal and replacement treatments. Further, immunohistochemical studies are in progress to examine the cellular marker of proliferation, ki67 and others. Taken together, the results suggest that E2 participates in regulation of CL function and IGFBP5 appears to be the potential molecule downstream of E2 signaling in the luteal function.

Nothing to Disclose: ST, MR

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