miR-506-3p regulates TGF- 1 and affects dermal fibroblast proliferation, migration and collagen formation after thermal injury.

Dermal fibroblasts are a promising candidate for cellular-based therapies for thermal wound healing because of their capacity of producing extracellular matrix (ECM), promoting wound contraction and the synthesis of type I collagen, and secreting growth factors. miRNAs (MicroRNAs) might mediate the role of TGF-β1(Transforming Growth Factor-beta 1), one of the major profibrotic cytokines, in improving thermal injury repair. In the present study, we observed the abnormal downregulation of TGF-β1 following thermal injury in the burnt dermis (in vivo) and heat-stimulated human dermal fibroblasts (in vitro). TGF-β1 overexpression reversed heat stimulation-induced repression on fibroblast viability, migration, and ECM synthesis. As demonstrated by online tool prediction and experimental analysis, miR-506-3p downregulated TGF-β1 levels via directly targeting TGFB1. In heat-stimulated human dermal fibroblasts, miR-506-3p expression showed to be significantly upregulated. miR-506-3p inhibition also reversed heat stimulation-induced repression on fibroblast viability, migration, and ECM synthesis; more importantly, TGF-β1 silencing aggravated the thermal injury in vitro and significantly reversed the effects of miR-506-3p inhibition on heat-stimulated dermal fibroblasts. In conclusion, miR-506-3p and its downstream target TGF-β1 form a regulatory axis, modulating the cell viability, migration, and ECM synthesis in human dermal fibroblasts following burn injury.