P53 expression in congenital experimental hydrocephalus induced by rat kidney antiserum

Abstract

Congenital hydrocephalus was induced by intraperitoneal administration of antipregnant rat kidney serum (APRKS) into rats at 9 days of pregnancy. To clarify a correlation between the oncogenes and expression of hydrocephalus, immunostaining of the fetal rat nervous system for p53 was carried out using Ab-1, a pantropic antirat p53 antibody, and Ab-3, raised against a mutant form of rat p53, Ab-1 staining was observed in cells of the neural plate of the fetus, the yolk sac, and the placenta. Because no staining occurred with Ab-3, it was likely that the p53 induced by antiserum injection was the wild-type protein. This result indicated that p53 may represent a reparative reaction to DNA damage from the APRKS; also, when DNA is irreparably damaged, p53 could induce apoptosis by favoring transcription of a gene encoding an inducet of apoptosis. Insufficient apoptosis, on the other hand, may induce failure of fetal development, contributing in particular to congenital hydrocephalus and other central nervous system anomalies.