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Updated: Jan 19, 2026
Murine Excisional Wound Healing Model and Histological Morphometric Wound Analysis
Published on: August 21, 2020
Anti-miR-200b promotes wound healing by regulating fibroblast functions in a novel mouse model
Renpeng Zhou1, Chen Wang1, Yimin Liang1
1Department of Plastic and Reconstructive Surgery, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
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.
Insights
MicroRNA-200b (miR-200b) significantly delays wound healing by impairing fibroblast function, including proliferation, migration, and collagen synthesis. This study introduces a novel murine plantar skin model for wound healing research.
Area of Science:
- Biomedical Science
- Dermatology
- Molecular Biology
Background:
- MicroRNA-200b (miR-200b) is downregulated in wound healing tissues.
- Fibroblasts are key cells in collagen production during wound repair.
- The role of miR-200b in regulating fibroblast function in wound healing remains unclear.
- Existing rodent wound models do not accurately mimic human skin structure.
Purpose of the Study:
- To investigate the effect of miR-200b on fibroblast function and wound healing.
- To establish and validate a murine plantar skin wound healing model.
- To explore the molecular mechanisms by which miR-200b influences wound repair.
Main Methods:
- Development of a murine plantar skin model with human skin-like anatomical features.
- In vivo gain- and loss-of-function studies of miR-200b in wound healing.
- In vitro assays to assess fibroblast proliferation, migration, and collagen synthesis.
- Analysis of Zeb1 expression levels.
Main Results:
- The murine plantar skin model demonstrated anatomical similarity to human skin.
- Overexpression of miR-200b significantly delayed wound healing in vivo.
- miR-200b reduced fibroblast proliferation, migration, and collagen synthesis.
- miR-200b decreased the expression of Zeb1.
Conclusions:
- miR-200b negatively regulates fibroblast functions critical for wound healing.
- miR-200b impairs wound healing by attenuating cell proliferation, migration, and collagen synthesis.
- The established murine plantar skin model is suitable for studying human skin wound healing.
- miR-200b's role in fibroblast regulation offers new insights into wound healing processes.
