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Published on: November 28, 2015
METTL14-mediated m6A methylation promotes macrophage M2 polarization via YTHDF1-Socs1 axis to accelerate skin wound
Jixun Zhang1, Chao Wang2, Xinxin Dong2
1Department of Plastic and Burn Surgery, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250033, People's Republic of China. jixunzhang@126.com.
Background:
Macrophage polarization plays a crucial role in the processes of inflammation, angiogenesis, and wound healing. N6-methyladenosine (m6A) RNA modification has been widely recognized as an abundant modification that regulates RNA expression. This work aimed to investigate the function of m6A modified Socs1 in skin wound healing.
Methods:
A full-thickness skin wounds mouse model was established and treated with Socs1 overexpression. The wound healing process and the histological changes of skin tissues were detected. Ana-1 macrophages were treated with lipopolysaccharide (LPS) to mimic the inflammatory environment during the wound healing process. The macrophage polarization was detected by immunofluorescence staining of specific biomarkers and production of inflammatory factors was measured using ELISA kits. Angiogenesis and fibroblast proliferation and migration were measured by the co-culture system of Ana-1 with dermal microvascular endothelial cells (DMECs) or dermal fibroblasts (DFs). The m6A modification of Socs1 mRNA was measured by m6A mRNA immunoprecipitation.
Results:
Socs1 expression was upregulated during wound healing process and M2 polarization of macrophages. Socs1 overexpression accelerated mouse skin wound healing and enhanced the formation of granulation tissue in wound tissues. Co-culture with Socs1-overexpressed macrophages increased angiogenesis of DMECs and enhanced the viability and migration of DFs. METTL14 regulates Socs1 expression in Ana-1 cells and increased the m6A methylation of Socs1 mRNA by recruiting YTHDF1.
Conclusion:
Socs1 regulates the M2 macrophages polarization and accelerates wound healing, which is modulated by METTL14-mediated m6A modification of Socs1 mRNA through YTHDF1 recruitment in macrophages.
Insights
N6-methyladenosine (m6A) modification of Socs1 mRNA accelerates skin wound healing by promoting M2 macrophage polarization. This process is regulated by METTL14 and YTHDF1 in macrophages.
Area of Science:
- * Molecular Biology
- * Immunology
- * Regenerative Medicine
Background:
- * Macrophage polarization is critical for inflammation, angiogenesis, and wound healing.
- * N6-methyladenosine (m6A) RNA modification regulates gene expression.
- * The role of m6A modified Socs1 in skin wound healing requires investigation.
Purpose of the Study:
- * To investigate the function of m6A modified Socs1 in skin wound healing.
- * To elucidate the regulatory mechanism of Socs1 m6A modification in macrophages.
Main Methods:
- * Established a full-thickness skin wounds mouse model with Socs1 overexpression.
- * Analyzed macrophage polarization using immunofluorescence and ELISA.
- * Assessed angiogenesis, fibroblast proliferation, and migration via co-culture systems.
- * Measured m6A modification of Socs1 mRNA using m6A immunoprecipitation.
Main Results:
- * Socs1 expression increased during wound healing and M2 macrophage polarization.
- * Socs1 overexpression accelerated wound healing and granulation tissue formation.
- * Socs1-overexpressed macrophages enhanced angiogenesis and fibroblast activity.
- * METTL14 and YTHDF1 were identified as key regulators of Socs1 m6A modification.
Conclusions:
- * Socs1 promotes M2 macrophage polarization and accelerates skin wound healing.
- * METTL14-mediated m6A modification of Socs1 mRNA, via YTHDF1 recruitment, is a key regulatory mechanism.
- * This study highlights the therapeutic potential of targeting m6A modification for wound healing.
