Expression of inhibin betaA, betaB and follistatin mRNAs in the carbon tetrachloride induced rat liver regeneration model.

Abstract

Follistatin (FS, an activin-binding protein) and activin A (homodimer of inhibin betaA chain) promote and inhibit cell proliferation in rat liver, respectively. The roles of activin AB (heterodimer of inhibin betaA and betaB) and activin B (homodimer of inhibin betaB) in rat liver have not been elucidated yet. In this study, we examined, by reverse-transcriptase polymerase chain reaction (RT-PCR) analysis, whether the levels of FS, inhibin betaA and betaB mRNAs change in the carbon tetrachloride induced rat liver regeneration model. The analysis was made in an hour-by-hour manner during the early stage of liver injury. There are 2 types of FS mRNA, FS-288 and FS-315, and the levels of both had begun to increase at 3 h, were maximal at 6 h, remained constant up to 12 h, and thereafter gradually decreased. The inhibin betaA mRNA had started to decline at 3 h, reached its lowest level at 6 h, partly returned at 12 h, and remained constant up to 48 h. The inhibin betaB mRNA level had begun to increase at 1 h, was maximal at 3 h, remained constant up to 24 h, and returned to the original level at 48 h. These results indicate that FS and activin A may act reciprocally in liver regeneration, and also suggest that activin AB and B may play roles in liver regeneration that differ from that of activin A.