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David G Simmons1 , Thomas G Kennedy1 *
Departments of Physiology and Obstetrics and Gynaecology, The University of Western Ontario, London, ON, Canada. 1
It has been well established that endometrial receptivity for implantation and sensitization for decidualization in rodents is a transient state under the control of the ovarian steroid hormones progesterone and estrogen. It is unclear, however, what molecular events mediate the hormonal control of the onset of uterine receptivity. Differential display (ddRT-PCR) was performed on total endometrial RNA obtained from ovariectomized rats treated with estradiol and progesterone to differentially sensitize their uteri for decidualization. Maximally sensitized uteri were at the equivalent of day 5 of pseudopregnancy, temporally nonsensitized uteri at days 4 or 6, and hormonally nonsensitized uteri from animals treated with low and high doses of estradiol. A cDNA with expression restricted to endometrium from maximally sensitized uteri was isolated, cloned and sequenced. The cDNA matched the sequence for rat GRP78 with 100% homology. GRP78 is a heat shock 70-related protein that resides in the ER lumen and has been shown to have a role in several different cellular processes such as multimeric protein assembly, the degradation of proteins, and the storage and regulation of ER luminal Ca2+. It has also been observed that some cells can express GRP78 on their cell surface and that it may play a role in the process of programmed cell death. Northern blot analysis indicated that GRP78 is dramatically up-regulated on day 5 of pseudopregnancy. Contrary to the ddRT-PCR findings, GRP78 mRNA also appeared to be induced in endometrium from animals treated with high doses of estrogen, suggesting that estrogen regulates the expression of this gene. Supported by the Medical Research Council of Canada.
This abstract is being presented on Sunday, August 1 at 8:00 AM to 10:15 AM at CUB 2nd Floor Ballroom.