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Biomedical subjects

H M Beier

Publications and source records attributed to H M Beier.

At least 109 records · Page 6Linked to original sources
PubMed1976

Uterine proteins and development in vitro of rabbit preimplantation embryos.

The effects of isolated protein fractions from rabbit uteri (prealbumin, albumin, uteroglobin, and beta-glycoprotein), unfractionated uterine proteins, progesterone, oestradiol-17beta, and prostaglandin F-2a on the development of rabbit embryos in vitro were investigated. When exposed to individual protein fractions obtained from Day-6 uteri, 8-cell embryos did not develop into early blastocysts; morulae readily developed into early blastocysts, but further development was retarded. Progesterone (10(-5)-10(-11)M) and prostaglandin F-2a (0-1-10 ng/ml) added to the medium slowed development of blastocysts to advanced stages. Growth of 8- to 16-cell embryos, morulae, and Day-4 blastocysts was stimulated by unfractionated uterine proteins obtained from Day-5 uterine flushings. Although embryos cultured in medium containing BSA had similar rates of blastocyst formation and, ultimately similar blastocyst expansion as did the embryos cultured in medium with unfractionated proteins, the radial and immediate expansion of the early blastocysts cultured in the latter approximated that found in utero.

Albumins↗
PubMed1976

Uteroglobin and related biochemical changes in the reproductive tract during early pregnancy in the rabbit.

The macromolecular secretion products of the rabbit uterus are described. The biochemical and biological properties of uteroglobin are considered, and its synthesis and secretion in various endocrinological conditions are described. The release of uteroglobin from the endometrial epithelium is stimulated by progestagens such as progesterone and its synthetic analogues, although its synthesis has not yet been shown to be entirely dependent on progesterone. The biological function of uteroglobin is obscure. Several approaches to this long-standing probelm are discussed, including the passage of uteroglobin into the blastocyst. It is suggested that interference with the passage of uterine components into the blastocyst may inhibit implantation and provide a means of contraception.

Animals↗
PubMed1975

Uteroglobin-like antigen in the male genital tract secretions.

The secretion of the rabbit seminal vesicle has been investigated by morphological and biochemical means. Apical regions of seminal vesicle epithelial cells show highly active protein synthesizing and releasing organells. The secretory proteins released are analysed by disc-electrophoresis and three different immunological procedures. There is evidence for the presence of an uteroglobin-like antigen in seminal vesicle secretion. Comparison with seminal plasma indicated that the uteroglobin-like protein is also present in this fluid. The immunological and electrophoretical identity of rabbit uteroglobin, obtained from the uterus, with "male uteroglobin" is obvious, but molecular-biochemical and biological identity awaits further clarification. The demonstration of uteroglobin-like antigen in the male as in the female points towards new aspects in reproductive and contraceptive research.

Animals↗
PubMed1975

Uteroglobin and other proteins in rabbit blastocyst fluid after development in vivo and in vitro.

Rabbit embryos were grown in vitro from the 2- and 4-celled stage to expanded blastocysts. Proteins from the blastocysts were analyzed for specific uterine proteins as well as for bovine serum albumin (BSA), a constituent of the medium. Immunological methods revealed the presence of rabbit albumin and larger amounts of BSA. Uteroglobin, the prevailing protein fraction present in blastocyst fluid of embryos that developed in vivo was not detected in blastocysts in vitro. Prealbumin and beta-glycoprotein were also absent. From the data presented, it appears that the blastocyst does not have the capacity to synthesize detectable concentrations of uterglobin and/or other specific uterine proteins.

Albumins↗
PubMedDate not supplied

Progestins, progesterone receptor modulators, and progesterone antagonists change VEGF release of endometrial cells in culture.

The influences of the synthetic progestin, medroxyprogesterone acetate (MPA), the progesterone receptor modulator J867, and the antagonist ZK137316 were studied in vitro on isolated endometrial epithelial cells, as well as endometrial fibroblasts. We evaluated the expression of estrogen receptor alpha (ER) and the progesterone receptor (PR) by RT-PCR. ER and PR were strongly expressed in the fibroblasts and epithelial cells under treatment with 10(-8) M 17beta-estradiol (E(2)). Treatment with 10(-6) M J867 or ZK137316 upregulated the PR expression as did E(2), in contrast to treatment with 10(-6) M MPA, which caused a downregulation of PR in epithelial cells, but not in fibroblasts. In addition, the vascular endothelial growth factor (VEGF) release into the cell culture medium was analyzed by a VEGF-ELISA. VEGF which plays an important role in angiogenesis, is regulated by steroid hormones as well as hypoxia. E(2) stimulates VEGF release into the medium in both cell types. MPA reduces VEGF release significantly in the fibroblast cell culture, but increases it in the epithelial cell culture. ZK137316, in the presence or absence of E(2), reduces VEGF release in fibroblast cell culture. J867 increases the VEGF production in fibroblasts only in the presence of E(2). Both compounds show no significant effects, compared to E(2), in epithelial cell culture. The different results for the epithelial cells and fibroblasts indicate that the pharmacological effects of PR modulators (PRMs) and progesterone antagonists (PAs) may be cell specific and depend on the presence or absence of partial progestagenic agonistic activities. This observation opens up new perspectives for various clinical applications.

Cell Culture Techniques↗
PubMedDate not supplied

The progesterone antagonist onapristone retards the advanced endometrial transformation after gonadotropin stimulation in rabbits.

Ovarian stimulation with gonadotropins (GN) during human in vitro fertilization and embryo transfer (IVF/ET) therapy alters the ovarian steroid output, especially that of progesterone. As a consequence, endometrial transformation is advanced, and embryo implantation is hampered. This study used the rabbit model to determine if the application of the progesterone antagonist (PA) onapristone (ONA) could retard endometrial development after GN-stimulation. Rabbits were GN-stimulated twice daily with 5 IU FSH and 5 IU LH on 3 consecutive days with a) hMG (n = 10) or b) with a mixture of recombinant FSH and LH (n = 10). The animals were then mated, and hCG was injected i.v. to ensure ovulation. This day is designated as day 0 post coitum (d 0 p.c.). On day 2 p.c., five animals of each group were treated with 20 mg ONA/kg body weight and five with vehicle for control. On d 5 p.c. endometrial transformation was analyzed by morphology, uteroglobin (Ugl)-mRNA expression, and proliferation. Embryos were flushed from the uteri. Their number and morphology was evaluated. The endometrium of GN-stimulated control animals demonstrated very long endometrial glands and narrow stromal septa. Ugl-mRNA expression was restricted to the cells at the bottom of the gland. 17.0 +/- 4.6% (mean +/- SD) of glandular cells and 6.0 +/- 5.3% of luminal epithelial cells proliferated. In ONA-treated animals, endometrial glands were significantly shorter, and the pattern of arborization was less pronounced. Endometrial gland cells and luminal epithelial cells expressed Ugl-mRNA. Furthermore, glandular and luminal cells proliferated with high intensity (38.6 +/- 6.8% and 36.4 +/- 9.3%, respectively). These results indicate that the status of endometrial differentiation was retarded after ONA-treatment. Nevertheless, the embryos of these ONA-treated animals were well developed. In conclusion, after GN-stimulation, ONA treatment retarded the advanced endometrial transformation in rabbits. Therefore, postovulatory administration of a PA might be a possible strategy to modulate the advanced endometrial development in IVF-cycles.

Animals↗