miR-23b promotes cutaneous wound healing through inhibition of the inflammatory responses by targeting ASK1

Area of Science:

• Molecular Biology
• Wound Healing Research
• Biomedical Science

Background:

• Wound healing involves inflammatory, proliferative, and remodeling phases.
• MicroRNAs (miRNAs) regulate skin trauma healing; altered expression links to abnormal healing.
• miR-23b's role in wound healing requires further investigation.

Purpose of the Study:

• To determine miR-23b expression variations post-trauma.
• To investigate miR-23b's therapeutic potential in accelerating wound healing.
• To elucidate the molecular mechanisms underlying miR-23b's function in wound repair.

Main Methods:

• Assessed miR-23b expression in mice and lipopolysaccharide-treated cells post-trauma.
• Evaluated wound healing acceleration in vivo with excessive miR-23b.
• Analyzed inflammatory cell infiltration, cytokine expression, and collagen synthesis.
• Investigated miR-23b's targeting of apoptotic signal-regulating kinase 1 (ASK1).

Main Results:

• Increased miR-23b significantly accelerated wound healing in vivo.
• miR-23b reduced inflammatory cell infiltration and suppressed pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, Ccl2) while increasing IL-10.
• miR-23b promoted α-SMA, Col1a1, and Col3a1 expression, indicating enhanced tissue repair.
• miR-23b inhibited inflammation by targeting ASK1, and ASK1 knockdown reduced inflammatory factors.

Conclusions:

• miR-23b is a potent therapeutic agent for cutaneous wound healing.
• miR-23b shortens inflammatory responses and promotes keratinocyte migration for re-epithelialization.
• Targeting miR-23b offers a promising strategy for improving wound healing outcomes.