HGF Accelerates Wound Healing by Promoting the Dedifferentiation of Epidermal Cells through -Integrin/ILK Pathway
Figure 3
HGF promotes ILK and c-met expression in scratched epidermal cells. (a) ILK and c-met expression in cultured epidermal cells was analyzed by western blot 48 h after scratch wounding. An increase of ILK and c-met expression was observed in epidermal cells treated with HGF (50 ng/mL) for 48 h. After epidermal cells were transfected with ILK siRNA, the expression of ILK and c-met was downregulated, despite the presence of HGF protein (50 ng/mL). (b) Graph represents densitometric analysis of western blots described in (a) ,. (c) The distribution of c-met, the receptor of HGF, was detected by IF. The c-met protein at the surface of the epidermal cells is green (white arrow) and in the nuclei is red (white triangle). (d) -Integrin and CK10 expression in scratched epidermal cells were tested by immunocytochemistry. HGF increased the expression of -integrin and downregulated CK10. However, ILK siRNA-transfected cells showed a significant knockdown of -integrin expression, with an increase in CK10 expression, compared to nontransfected or control cells. (e) Graph represents densitometric analysis of western blot described for (d) , . The results revealed that there was a statistically significant difference between HGF group versus normal and HGF + siILK groups. All these suggested that HGF could activate the -integrin and ILK signaling pathway; inversely, -integrin and ILK might regulate the expression and function of HGF/c-met.
