An in vitro study of teratogenicity in the rat due to antibody-induced yolk sac dysfunction

Archiv für Entwicklungsmechanik der Organismen - Tập 195 - Trang 236-242 - 1986
Stuart John Freeman1, Nigel Andrew Brown1
1MRC Experimental Embryology and Teratology Unit, Medical Research Council Laboratories, Carshalton, UK

Tóm tắt

An antiserum was prepared in rabbit against rat visceral yolk sac endoderm. The initial injection was of a ConA-Sepharose purified fraction of endoderm, and subsequent injections were of whole endoderm. The antiserum was found to be a potent rat teratogen in vivo, the most common defects observed being anophthalmia and hydrocephaly. Using rat whole embryo culture, the antiserum was demonstrated to induce dysmorphogenesis and growth retardation in a concentration dependent manner. The most frequent abnormalities were of the optic primordia, suggesting a similar embryonic response in vitro to that observed in vivo. In further culture experiments, the antiserum was shown to inhibit macromolecule (125I-labelled PVP) uptake by the visceral yolk sac, an essential process in embryonic nutrition. This effect of impaired yolk sac-mediated nutrition confirms previous observations using anti-whole yolk sac antiserum (Freeman et al. 1982), and it is proposed as the primary cause of teratogenesis. In order to identify the yolk sac antigen(s) involved in the teratogenic response, yolk sac endoderm peptides were separated by PAGE and electrophoretically transferred to nitrocellulose for analysis. With an enzyme linked immunoassay, the antiserum was observed to cross-react with a single 30 kd peptide, demonstrated by a ConA-binding technique to be a glycopeptide. Control serum showed no evidence of cross-reaction with yolk sac peptides.

Tài liệu tham khảo

Freeman SJ, Brown NA (1985a) Identification of a ConA-binding glycoprotein of rat visceral yolk sac endoderm involved in antiyolk sac antiserum teratogenesis. Teratology 31:43A

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