Expression of Hsp47 in Fibroblasts Derived from Fetal and Neonatal Rat Tongues

Scar formation, caused by the abnormal expression and accumulation of collagen molecules accompanying the expression of heat shock protein 47 (Hsp47), a collagen-specific molecular chaperone, is a serious problem after surgery in the postnate, whereas in the fetus, the wound heals without scarring. In this study, we compared the expression patterns of Hsp47 and type I and type III collagens induced by TGF-β1 between fetal and neonatal fibroblasts in the primary cultures of rat tongues. In the neonate, high level expressions of both Hsp47 and collagen mRNAs and proteins were observed to be induced by TGF-β1, but not in the fetus. We performed a reporter assay using pLUC 5.5 (III), which carried the enhancer/promoter region of the mouse Hsp47 gene, to compare promoter/reporter activity. In the neonate, high promoter/ reporter activity in fibroblasts treated with TGF-β1 was observed, but was unchanged in the fetus. Thus, the expression of Hsp47 is enhanced by TGF-β1 in the neonate but not in the fetus. This different Hsp47 expression pattern between the fetus and neonate appears to be attributed to the different transcriptional regulation of the gene. Elucidation of the regulatory mechanism of Hsp47 production in developmental processes may provide a therapeutic modality for the scarless healing of postnatal wounds.