Rescue of Dvl3-DEP Peptide on rpS6 Induced Seminiferous Epithelium Injury in Rat Testis

In order to determine the rescue effect of Dvl3-DEP peptide on rpS6 induced testicular seminiferous epithelium injury in rats and its potential mechanism, the rat testicular overexpression animal model was used. Seminiferous epithelium injury was induced by rpS6 tetraphosphorylation mutant overexpression, furthermore, DEP peptide was overexpressed in testis. The mechanism of DEP peptide rescue rpS6 induced seminiferous epithelium injure was then analyzed. The permeability of blood testis barrier, damage of seminiferous epithelium, cytoskeleton structures and its aggregation ability, and expression of cytoskeleton regulatory proteins were detected. Results showed that DEP peptide could effectively rescue rpS6 induced damage on the blood testis barrier and significantly reduce the proportion of seminiferous tubule injury. Phalloidin and immunofluorescence staining of actin and tubulin from testis sections showed that DEP overexpression effectively maintained the functional structure of cytoskeleton proteins. Furthermore, DEP overexpression could effectively maintain the aggregation levels of actin and tubulin in tissues. The up-regulated expression of actin regulatory protein Eps8 and down-regulated expression of tubulin regulatory protein MARK4 suggested that DEP renovated rpS6 induced cytoskeletal structure damage through the expression differences of the above two regulatory proteins. The study confirmed the protective effect of DEP peptide on seminiferous epithelium function, and creatively used rpS6 tetraphosphorylation mutant as the model of testicular injury induction, which provided a reference for the research of animal testicular injury therapy and drug development.

CSTR: 32200.14.cjcb.2022.10.0002