Unique endometriosis-specific secretory proteins would be of paramount importance as noninvasive markers for diagnosis and evaluation of therapeutic approaches for endometriosis. Furthermore, identification of endometriosis-specific secretory proteins may be an important step towards understanding the pathophysiology of endometriosis-associated pain and infertility. Therefore this study was designed to assess protein synthesis and secretion by ectopic uterine implants from steroid-treated and reproductively cyclic rats with surgically induced endometriosis. Uteri, ectopic uterine implants, and control tissues were incubated in L-[35S]methionine or D-[6-3H]glucosamine for 0-24 h and 24-48 h. De novo-synthesized proteins released into the culture media were identified using two-dimensional SDS-PAGE, fluorography, and computer-assisted image analysis. Two distinct groups of ectopic uterine implant proteins were identified: ENDO I (M(r) 40,000-50,000; pI 4.0-5.2) and ENDO II (M(r) 28,000-32,000; pI 7.5-9.0) were produced by ectopic uterine implants and not the uteri. A third group of proteins, previously identified in culture media of the uteri from progesterone-treated rats and called PUP-1 (M(r) 70,000; pI 5.7), was synthesized and secreted by ectopic uterine implants 24-48 h later than in parallel uterine cultures. The detection of ectopic uterine implant proteins suggests biochemical characteristics of the ectopic tissue that may be used to develop unique markers for endometriosis. Furthermore, the delayed synthesis and secretion of the uterine protein PUP-1 by the ectopic uterine implants illustrates yet another example of the asynchronous behavior of these two tissues, which may be related to the etiology or pathophysiology of the disease.
The proportions of Type I and Type III collagen were evaluated from gestational, postpartum-retained, and released bovine placental membranes. Placentomes were excised at 90, 150, 210, and 270 days of gestation (n = 32) and from postpartum-retained (2 and 12 h, n = 8) and released (2 h, n = 4) membranes. Placentome components were processed for collagen, hydroxyproline, protein, and dry weight determination. Collagen extracts were separated by SDS-PAGE. Densitometry was used to establish the proportions of collagen alpha chains (Type I = 2 alpha 1 + 1 alpha 2; Type III = 3 alpha 1). No difference in the proportion of maternal caruncular Type I and Type III collagen was found. The proportion of Type I fetal cotyledonary collagen was lowest (p less than 0.05) at Day 90 of gestation but did not differ between Days 150, 210, 270, or between retained and released fetal membranes. The proportion of Type III fetal cotyledonary collagen was greatest (p less than 0.05) at Day 90. Retained fetal cotyledons had a greater (p less than 0.05) proportion of Type III collagen than did released fetal cotyledons. Therefore, although hydroxyproline content was not different between retained and released fetal membranes, the retained bovine fetal cotyledon was characterized by disproportionate amounts of Type III collagen as compared to the fetal cotyledon that was not retained.
Adverse effects of the GnRH antagonist Antide on folliculogenesis and fertility were noted when we were evaluating the therapeutic value of Antide on endometriosis in a rat model. Cyclic rats with (n = 56) and without (n = 18) surgically induced endometriosis received Antide (2 mg/kg) or vehicle at noon on days 0 (proestrus), 3, 6, and 9. Rats were killed at noon on days 0, 6, 12, 18, 24, 30, 42, and 165. The number of antral follicles and the number of atretic antral follicles evaluated did not differ (P greater than 0.05) between endometriosis and control rats. Antide-treated rats had more (P less than 0.05 ) atretic antral follicles (64.7%) than vehicle-treated rats (15.3%). Antide-treated rat ovaries contained fewer corpora lutea than those of vehicle-treated rats on days 6, 12, and 18. No corpora lutea were found in Antide-treated rat ovaries after day 18. The abnormal ovarian morphology of the Antide-treated rats persisted for the duration of the project (165 days). Fertility (rats without endometriosis) was assessed by mating vehicle-and Antide-treated rats at spontaneous proestrus (n = 8) for eight posttreatment cycles as well as after follicular stimulation (n = 2). All vehicle-treated and no Antide-treated rats became pregnant. No oocytes were found in the oviducts of Antide-treated rats after eight cycles, indicating that ovulation had not occurred. The serum FSH and estradiol concentrations in the rats treated with Antide were lower (P less than 0.05) on days 6, 12, and 18, but rose to values equal to (days 24 and 30) or greater than (day 42) those in vehicle-treated rats. Serum progesterone levels in rats treated with Antide were lower (P less than 0.05) than those in vehicle-treated rats on all days tested. In conclusion, at a dosage sufficient to suppress reproductive cyclicity (and elicit the regression of endometriosis), Antide also caused long term follicular atresia and infertility.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.