Evaluation of the role of TGFβ, a-SMA and FGF۱ genes in scar formation during wound healing

Background and Aim: When there is a physical injury to the skin, homeostatic turnover of the skin is temporarily halted and switches instead to a wound healing and reparative response. Keloids and hypertrophic scars are suboptimal consequences of skin wound healing, and are believed to be unique to human skin. Fibroblasts and myofibroblasts are important cells in the wound healing and scar formation.Methods: In this study we focused on some alternative mechanisms involved in pathways that regulate formation of scars. Reactome and STRING servers were used for collection of previously reported pathways. In our research, a-SMA, TGFβ and FGF۱ genes were considered as the core molecules and finally pathways were linked together by application of Cytoscape software.Results: Our presented pathways can mapped the core molecules that considered in this study. In this web mapping analysis, we showed the location of our favorite genes in scar generation. Fibroblasts acquire contractile stress fibers with alpha-smooth muscle actin (α-SMA) thus forming the “myofibroblast”. Expression of a-SMA is precisely controlled by the joint action of growth factors like transforming growth factor (TGFb۱).Conclusion: This results may be useful for development of new strategies for skin care medicine.

Keywords:

Wound healing , scar formations , web mapping , pathways.