| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 4351421 | Neuroscience Research | 2013 | 9 Pages |
•Traumatic spinal cord injury causes immediate loss of vascular support.•The wound healing response after injury requires expression of wound healing/angiogenesis-related proteins.•VEGF is a potent stimulator of angiogenesis and protects neurons from death.•VEGF leads to vessel permeabilization and thus a ‘leaky’ blood-spinal cord barrier.
Patients with spinal cord injury (SCI) are permanently paralysed and anaesthetic below the lesion. This morbidity is attributed to the deposition of a dense scar at the injury site, the cellular components of which secrete axon growth inhibitory ligands that prevent severed axons reconnecting with denervated targets. Another complication of SCI is wound cavitation where a fluid filled cyst forms in the peri-lesion neuropil, enlarging over the first few months after injury and causes secondary axonal damage. Wound healing after SCI is accompanied by angiogenesis, which is regulated by angiogenic proteins, produced in response to oxygen deprivation. Necrosis in and about the SCI lesion sites may be suppressed by promoting angiogenesis and the resulting neuropil protection will enhance recovery after SCI. This review addresses the use of angiogenic/wound-healing related proteins including vascular endothelial growth factor, fibroblast growth factor, angiopoietin-1, angiopoietin-2 and transforming growth factor-β to moderate necrosis and axon sparing after SCI, providing a conducive environment for growth essential to functional recovery.
