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PRMT1-rich exosomes derived from M2 macrophages as novel therapeutics for enhancing fracture healing

Haifeng Hong1, Cuiyun Zhou2, Haibing Wang1

  • 1Department of Orthopedics, Fuzhou First General Hospital Affiliated with Fujian Medical University, Fuzhou, Fujian 350000, China.

Tissue & Cell
|January 29, 2026
PubMed
Abstract

Insights

Macrophage-derived exosomes (M2-Exo) deliver protein arginine methyltransferase 1 (PRMT1) to bone marrow mesenchymal stem cells (BMSCs), enhancing bone healing. PRMT1 promotes osteogenic differentiation by modifying Sam68, offering a therapeutic strategy for fracture repair.

Area of Science:

  • Biomaterials Science
  • Regenerative Medicine
  • Cell Biology

Background:

  • Macrophage-derived exosomes (M2-Exo) show potential in bone repair due to anti-inflammatory and regenerative properties.
  • The precise molecular mechanisms of M2-Exo interaction with bone marrow mesenchymal stem cells (BMSCs) require further investigation.
  • Previous research identified protein arginine methyltransferase 1 (PRMT1) in exosomes as a promoter of bone healing.

Purpose of the Study:

  • To investigate the osteoprotective effect of PRMT1-containing M2-Exo during fracture healing.
  • To elucidate the underlying molecular mechanisms of M2-Exo's action on BMSCs.

Main Methods:

  • PRMT1 was knocked down in M2-Exo, which were then used to treat BMSCs.
  • Osteogenic differentiation was assessed using qRT-PCR, western blot, Alizarin Red S, and Alkaline phosphatase (ALP) assays.
  • Immunoprecipitation was used to study the interaction between PRMT1, Sam68, and its ADMA modification.

Main Results:

  • PRMT1 delivered by M2-Exo enhanced BMSC osteogenic differentiation, evidenced by increased mineralization and ALP activity.
  • Knockdown of PRMT1 in M2-Exo suppressed osteogenic differentiation and reduced BMP2 and RUNX2 expression.
  • PRMT1 interacted with Sam68, and this interaction was crucial for ADMA modification and osteogenic gene expression; Sam68 overexpression partially rescued PRMT1 knockdown-induced defects.

Conclusions:

  • M2-Exo-derived PRMT1 enhances BMSC osteogenic differentiation by catalyzing Sam68 ADMA modification.
  • These findings support the potential of M2-Exo as a therapeutic agent for improving bone healing.
  • The study provides a mechanistic understanding of M2-Exo's role in fracture repair.
Keywords:
ExosomesFracture healingM2 macrophagesMethylationPRMT1

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