Figure 2.

Temporal changes and treatment in spinal cord injury. (a) IFN-γ and LPS-TLR4 induce microglia to switch to M1 type within 3 days of injury and secrete TNF-α, IL-1β, IL-6 and IL-12. IL-4, IL-13, IL-10 and TLRs stimulate the switch to M2 type, which secrete IL-10 and IL-13. The M1 type eventually dominates. (b) OPCs/NG2 can differentiate into Schwann cells and astrocytes in the early stage of injury, or these can differentiate into oligodendrocytes and express NG2, PDGFRα and GFAP. (c) Astrocytes transform into reactive astrocytes after injury and up-regulate the expression of GFAP, nestin, vimentin, Nes, Ctnnb1, Axin2, Plaur, Mmp2 and Mmp13; however, over 2–4 weeks, A1-like astrocytes appear and up-regulate Cdh2, Sox9, Xylt1, Chst11, Csgalnact1, Acan, Pcan, Slit2 and another type of scar that secretes TNF-α, IL-1, IL-6, FGF and NGF. (d) Therapeutic strategy: surgical treatment, high-dose methylprednisolone, cell (iPS, BMSC, Schwann cell, neonatal microglia, embryonic stem cells, olfactory nerve sheath cells) transplantation, cocktail therapy, transforming astrocytes into neurons. IFN-γ interferon-gamma, TNF- α tumor necrosis factor-alpha, IL interleukin, OPCs oligodendrocyte progenitor cells, GFAP glial fibrillary acidic protein, FGF fibroblast growth factor, NGF nerve growth factor