Anti-miR-200b promotes wound healing by regulating fibroblast functions in a novel mouse model.

Abstract

MicroRNA-200b (miR-200b) down-regulation has been found in wound-healing tissues. Fibroblasts are the predominant cells that orchestrate the production of collagen in wound healing. However, it is still unclear whether miR-200b can affect the wound healing by regulating the fibroblasts' function. The current rodent wound-healing models are not ideal due to their marked difference in structure compared with the human skin. In this study, we demonstrated that the murine plantar skin had similar anatomical features to the human skin. Using this model, the gain/loss-of-function studies showed that miR-200b caused a significantly delayed wound healing in vivo. Furthermore, using cell proliferation, migration and collagen synthesis assays, we found that miR-200b attenuated cell proliferation, migration and collagen synthesis of fibroblasts, which are critical aspects of wound healing. miR-200b also decreased the expression of Zeb1. Collectively, we established a new murine plantar skin model for the investigation of wound healing, and based on it we found that miR-200b affected the wound healing by regulating the biological function of fibroblasts, which provided a new insight for wound healing.