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Prmt6 Deficiency or Inhibition Restores Microglial Homeostasis and Promotes Scar-Limited Repair in Adult Spinal Cord
Weilin Peng1, Zhengqiang Wu1, Yu Xiong1
1Department of Orthopaedics, Changzheng Hospital, Naval Medical University, Shanghai, China.
Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|April 17, 2026
Summary
Neonatal mice heal spinal cord injuries scar-free by maintaining microglial balance. Inhibiting protein arginine methyltransferase 6 (PRMT6) in adults restores this balance, reduces scarring, and promotes nerve repair.
Area of Science:
- Neuroscience
- Immunology
- Epigenetics
Background:
- Adult spinal cord injury (SCI) healing is impaired by persistent microglial dyshomeostasis and scar formation.
- Neonatal mice exhibit scar-free healing, suggesting mechanisms to restore microglial homeostasis are key.
Purpose of the Study:
- To identify regulators of microglial homeostasis differences between neonatal and adult SCI.
- To investigate the role of protein arginine methyltransferase 6 (PRMT6) in adult SCI scar formation and repair.
Main Methods:
- RNA sequencing to identify key regulators in microglia.
- Genetic manipulation (Prmt6 deficiency, knockdown) and pharmacological inhibition of PRMT6 in adult mice.
- Assessment of microglial markers (P2Y12, TMEM119, CD68), scar formation, axonal regrowth, and motor function.
Main Results:
- PRMT6 is upregulated in adult microglia post-SCI but low in neonates.
- Prmt6 deficiency or inhibition in adult mice restored microglial homeostasis, reduced scarring, and improved axonal regrowth and motor recovery.
- PRMT6 epigenetically represses PGC-1α expression by depositing H3R2me2a, inhibiting fatty acid oxidation (FAO) and disrupting microglial homeostasis.
Conclusions:
- PRMT6 is a critical epigenetic regulator linking microglial metabolic dysfunction and maladaptive scarring in adult SCI.
- Targeting PRMT6 offers a potential therapeutic strategy to reprogram microglial metabolism and enhance neural repair after SCI.
