Inhibition of HDAC6 promotes microvascular endothelial cells to phagocytize myelin debris and reduces inflammatory response to accelerate the repair of spinal cord injury

Spinal cord injury (SCI) leads to myelin sheath damage, causing inflammation that hinders SCI repair. Microvascular endothelial cells (MECs) can remove myelin debris, but this can also increase inflammation. This study explores how inhibiting HDAC6, an enzyme, affects MECs' ability to clear myelin debris and reduce inflammation after SCI. The study uses a coculture model of myelin debris and vascular-like structures. The researchers found that inhibiting HDAC6 promotes MECs to clear myelin debris, reduces inflammatory factors, and accelerates SCI repair. This suggests a new treatment strategy for SCI.

• 1
  MECs phagocytize myelin debris via IgM opsonization, which promotes secretion of inflammatory factors. IgG-opsonized myelin debris does not have the same effect.
• 2
  Tubastatin-A, an HDAC6 inhibitor, increased IgG levels and decreased IgM levels by regulating B cell proliferation and differentiation.
• 3
  Inhibition of HDAC6 regulates the autophagy-lysosome pathway, promoting MECs to phagocytize myelin debris and reducing inflammatory factors.