Uterine proteins and development in vitro of rabbit preimplantation embryos

Abstract

Summary. The effects of isolated protein fractions from rabbit uteri (prealbumin, albumin, uteroglobin, and \g=b\-glycoprotein),unfractionated uterine proteins, progesterone, oestradiol-17\g=b\, and prostaglandin F-2\g=a\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\ p=n-\ 5\ p=n-\ 10\ p=n-\ 11m) and prostaglandin F-2\g=a\(0\m=.\1\p=n-\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.

Development retardation in cultured preimplantation rabbit embryos

“…In all these studies, treatment of uterine flushings by dialysis, lyophilization, fractionation, storage, or adjustment to a given protein concentration was involved. In most cases, best development occurred in unfractionated uterine flushings (El-Banna & Daniel, 1972b;Maurer & Beier, 1976;Beier et ai, 1983 Guilbert-Blanchette & Lambert (1978) found almost the same percentage of rabbit morulae developed into blastocysts in flushings derived from 'oestrous' or pseudopregnant rabbits of different times after hCG.…”

“…Although various developmental stages and criteria have been examined, supplementation of culture media with uterine secretions is consistently reported to improve development of cul¬ tured rabbit embryos (Gulyas et ai, 1969;El-Banna & Daniel, 1972a, b;Maurer & Beier, 1976;McCarthy et ai, 1977;Guilbert-Blanchette & Lambert, 1978;Beier et ai, 1983). In all these studies, treatment of uterine flushings by dialysis, lyophilization, fractionation, storage, or adjustment to a given protein concentration was involved.…”

“…Retardation, e.g. in rabbit embryos, is manifest both in quantitative terms such as cell number or embryo size (Pincus & Werthessen, 1938;Seidel, 1960;Daniel, 1967; Staples, 1967;Onuma et ai, 1968;Adams, 1970;Anderson & Foote, 1975;Maurer & Beier, 1976; Kane & Headon, 1980; Kane, 1985;Stroebele-Mueller et ai, 1985) and qualitative terms like developmental delay before transfer (Seidel et ai, 1976) or embryoblast differentiation (Beier et ai, 1983). The aim of the present study was to characterize further and quantify in-vitro retardation by using the technique of thymidine incorporation.…”

Purification of human alpha uterine protein

“…This protein, which is also known as uteroglobin (Beier, 1968(Beier, , 1974 and cone protein (Feigelson, 1976), was thought to induce cavitation in rabbit blastocysts in vitro (Krishnan & Daniel, 1967). Although this conclusion has been disputed by Maurer & Beier (1976), blastokinin may still have some indirect embryotrophic effect, perhaps associated with its postulated role as a progesterone carrier (Beier, 1976;Beato, 1977). Despite higher initial estimates by Krishan & Daniel (1968), the molecular weight of blastokinin is now accepted to be approximately 15 000 by gel filtration (Kay & Feigelson, 1972;Daniel, 1976).…”

Administration of the nonsteroidal anti-inflammatory drug tolfenamic acid at embryo transfer improves maintenance of pregnancy and embryo survival in recipient mice

“…Since PGF2α is the main hormone that triggers luteolysis [7], it could indirectly cause embryonic loss before maternal recognition of pregnancy. Furthermore, addition of PGF2α to the culture medium has shown to inhibit in vitro development of rabbit [8] and bovine embryos [9]. Thus, in mammalian females the inhibition of endometrial PGF2alpha release or the blockage of its action contributes to maintain luteal function, embryo survival and establishment of pregnancy.…”