Highlights

• Extensive oligodendrocyte death during the first two weeks after TSCI leave a broad number of denuded axons.
• OPCs start proliferation at the lesion borders and spared tissues as early as one day after injury.
• Within the first two weeks after injury the proliferation rate of OPCs reaches to a maximum.
• Differentiation of newly formed OPCs compensates the lack of oligodendrocyte.
• OPC-derived Schwann cells as well as invading peripheral Schwann cells also contribute in remyelination after TSCI.

In an experimental study, the potentiality of the IKVAV-functionalized hydrogel was explored to provide a permissive environment for cell migration and growth as well as sustained release of BDNF at the lesion after severe compression injury in rats.

Although the locomotor functional recovery was not observed, the axon preservation and minimal inflammation in animals treated with BDNF incorporated hydrogel indicate the potentiality of the designed intervention for further evaluations in the path of developing efficient therapies for severe spinal cord injury.