siRNA-Mediated MELK Knockdown Induces Accelerated Wound Healing with Increased Collagen Deposition

Skin wounds remain a significant problem for the healthcare system, affecting the clinical outcome, patients' quality of life, and financial costs. Reduced wound healing times would improve clinical, economic, and social aspects for both patients and the healthcare system. Skin wound healing has been studied for years, but effective therapy that leads to accelerated wound healing remains to be discovered. This study aimed to evaluate the potential of MELK silencing to accelerate wound healing. A vectorless, transient knockdown of the MELK gene using siRNA was performed in a murine skin wound model. The wound size, total collagen, type 3 collagen, vessel size, vessel number, cell proliferation, cell apoptosis, number of mast cells, and immune infiltration by CD45, CD11b, CD45, and CD8a cells were evaluated. We observed that treatment with MELK siRNA leads to significantly faster wound closing associated with increased collagen deposition.

Automated summary

Skin wounds are a significant problem for the healthcare system, impacting clinical outcomes, patient quality of life, and financial costs. Faster wound healing could benefit both patients and the healthcare system in terms of clinical, economic, and social aspects. This study aimed to assess the potential of MELK silencing in accelerating wound healing. MELK siRNA treatment was found to lead to faster wound closure and increased collagen deposition.