Differential gene regulation by estrogen and progesterone in the primate endometrium.
During the shift from a proliferative to a secretory endometrium in the rhesus menstrual cycle, progesterone action causes massive metabolic and structural remodelling. In order to identify genes whose expression is potentially important for the change from estrogen (E) to progesterone (P) dominance we have initiated a study of specific gene regulation using semiquantitative, reverse transcription polymerase chain reaction (RT-PCR). PolyA+ RNA was isolated from both E-dominant (days 9-13 of artificial menstrual cycles [AMCs]) and P-dominant (days 21-23) rhesus monkey endometria. The two pools of mRNA were converted to cDNA, end-ligated to double-stranded oligonucleotide adaptors and amplified by PCR using an adaptor-complementary primer. This procedure resulted in the production of E- and PcDNA template populations for cDNA-specific screening and comparative quantitation by PCR. Initial analysis showed that placental protein 14 (PP14) was P-dependent and human complement 3 (HC3) was up-regulated in E-dominant tissue, whereas the housekeeping genes B-actin and glyceraldehyde-3-phosphate dehydrogenase (G-3-PDH) were expressed at equivalent levels under E and P dominance. Expression of the E receptor (ER), P receptor (PR), epidermal growth factor receptor (EGFR) and insulin-like growth factor (IGF-I) was equivalent under E or P dominance. Expression of epidermal growth factor (EGF) and retinoblastoma (RB) was down-regulated in P-dominant tissue. Conversely IGF-1 receptor (IGF-1-R), transforming growth factor-beta 2 (TGFB-2), TGFB-2 receptor (TGFB-2-R), 17 beta-hydroxysteroid dehydrogenase (17-B-HSD) and leukemia inhibitory factor (LIF) levels were up-regulated in PcDNA. Among these factors, PP14, LIF, IGF-1-R TGFB-2 and 17-B-HSD were also detectable in PCR in a P-dependent cDNA library isolated by subtractive hybridization. These data provide evidence for hormonal regulation of specific gene products that may play important roles in the normal maturation of the primate endometrium in preparation for implantation.
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Department of Obstetrics and Gynecology, University of Massachusetts Medical School, Worcester 01655, USA.
Okulicz
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D000818:Animals; D001483:Base Sequence; D017931:DNA Primers / Q000235:genetics; D018076:DNA, Complementary / Q000235:genetics; D004717:Endometrium / Q000187:drug effects / Q000378:metabolism*; D004815:Epidermal Growth Factor / Q000235:genetics / Q000378:metabolism; D004958:Estradiol / Q000378:metabolism* / Q000494:pharmacology; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D006728:Hormones / Q000235:genetics / Q000378:metabolism; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000235:genetics / Q000378:metabolism; D008253:Macaca mulatta; D008597:Menstrual Cycle / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D008969:Molecular Sequence Data; D016133:Polymerase Chain Reaction; D011374:Progesterone / Q000235:genetics* / Q000494:pharmacology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D011960:Receptors, Estrogen / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D011980:Receptors, Progesterone / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism
D017931:DNA Primers; D018076:DNA, Complementary; D006728:Hormones; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D016212:Transforming Growth Factor beta; D011374:Progesterone; D004958:Estradiol; D004815:Epidermal Growth Factor; D007334:Insulin-Like Growth Factor I