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Purpose <p>Adipose-derived mesenchymal stem cells (ADSCs) exosomes (AD-Exos) are a novel andpromising therapeutic approach for skin damage repair. This investigation seeks to assess the potentialclinical utility of miR-141-3p found in AD-exos for expediting wound healing.</p> Methods <p>ADSCs wereisolated from the wounded patients’ tissue and validated via flow cytometry, and the mineralization andadipogenic capabilities of ADSCs were assessed respectively. Additionally, exosomes were isolated andidentified. miR-141-3p and HDAC6.protein level were tested. Full-thickness wound models were createdon the backs of mice, HE staining, ELISA, and immunohistochemistry were used to assess the influencesof AD-exos on wound healing, inflammation, and new blood vessel formation Western blot was to assessthe related-protein levels of JNK/ERK pathway. AQ1 Meanwhile, Dual-Luciferase assay confirmed therelationship between miR-141-3p and HDAC6.</p> Results <p>The isolated cells highly express surfacemarkers of mesenchymal stem cells and possess the potential for multidirectional differentiation,confirming them to be ADSCs. And miR-141-3p down-regulated but HDAC6 up-regulated in the serumand AD-exos of wounded patients. miR-141-3p could negatively modulate HDAC6. The miR-141-3p inAD-exos accelerated wound healing in mice, mitigated inflammatory responses and scarring in theinjured skin tissue, and promoted angiogenesis, moreover, AD-exos could diminish the phosphorylationof JNK and ERK, while HDAC6 overexpressed could weaken these impacts.</p> Conclusion <p>miR-141-3p in AD-exos can target down regulate HDAC6 expression and inhibit JNK/ERK signalingpathway activation, thereby reducing wound inflammation and promoting angiogenesis and woundhealing in mice.</p> Graphical Abstract <p>In exosomes isolated from ADSCs cells, miR-141-3p can target and negatively regulate HDAC6 expression, thereby inhibiting the activation of JNK/ERK signaling pathway, promoting wound healing and reducing scar formation.</p> <p></p>

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The efficacy of miR-141-3p to facilitate the healing of wounds and prevent scarring in mice by blocking the JNK/ERK pathway via HDAC6 silencing

  • 期刊论文

  • 发表日期：

    2025年2月15日

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  • YunTong Zhang,
  • XuHui Wang,
  • ZiShuo Wang,
  • JianGuo Xu,
  • Miao Xu,
  • JieSong Zhou,
  • Shuo Fang

摘要

Purpose

Adipose-derived mesenchymal stem cells (ADSCs) exosomes (AD-Exos) are a novel andpromising therapeutic approach for skin damage repair. This investigation seeks to assess the potentialclinical utility of miR-141-3p found in AD-exos for expediting wound healing.

Methods

ADSCs wereisolated from the wounded patients’ tissue and validated via flow cytometry, and the mineralization andadipogenic capabilities of ADSCs were assessed respectively. Additionally, exosomes were isolated andidentified. miR-141-3p and HDAC6.protein level were tested. Full-thickness wound models were createdon the backs of mice, HE staining, ELISA, and immunohistochemistry were used to assess the influencesof AD-exos on wound healing, inflammation, and new blood vessel formation Western blot was to assessthe related-protein levels of JNK/ERK pathway. AQ1 Meanwhile, Dual-Luciferase assay confirmed therelationship between miR-141-3p and HDAC6.

Results

The isolated cells highly express surfacemarkers of mesenchymal stem cells and possess the potential for multidirectional differentiation,confirming them to be ADSCs. And miR-141-3p down-regulated but HDAC6 up-regulated in the serumand AD-exos of wounded patients. miR-141-3p could negatively modulate HDAC6. The miR-141-3p inAD-exos accelerated wound healing in mice, mitigated inflammatory responses and scarring in theinjured skin tissue, and promoted angiogenesis, moreover, AD-exos could diminish the phosphorylationof JNK and ERK, while HDAC6 overexpressed could weaken these impacts.

Conclusion

miR-141-3p in AD-exos can target down regulate HDAC6 expression and inhibit JNK/ERK signalingpathway activation, thereby reducing wound inflammation and promoting angiogenesis and woundhealing in mice.

Graphical Abstract

In exosomes isolated from ADSCs cells, miR-141-3p can target and negatively regulate HDAC6 expression, thereby inhibiting the activation of JNK/ERK signaling pathway, promoting wound healing and reducing scar formation.