Disruption of the blood-spinal cord barrier (BSCB) and microvascular changes leading to reduction of blood supply represent hallmarks of spinal cord secondary injury causing further deterioration of the traumatized patient. Injury to the blood vessels starts with prominent hemorrhage and generation of inflammation. Furthermore, spinal cord ischemia and extravasation of blood components contribute to edema formation resulting in death of neural cells. Endogenous attempts of re-vascularization have been observed although these newly formed vessels display morphological and functional abnormalities. The unfavorable regulation of angiogenic and counterregulatory anti-angiogenic factors during the complicated course of vessel remodeling after SCI is suspected to participate in the failure of re-vascularization and vessel stabilization. Repression of the expression of angiogenic factors such as vascular endothelial growth factor-A (VEGF-A), placental growth factor (PlGF), angiopoietin-1 (Ang1), and platelet-derived growth factor-BB (PDGF-BB) contributes to vessel regression. Therefore, therapeutic applications of angiogenic factors following SCI are promising strategies to restore blood flow in the lesion.
Keywords: Angiogenic factors, angiogenesis, blood vessels., cell-based therapy, re-vascularization, spinal cord injury, blood-spinal cord barrier (BSCB), autoregulation, small anastomoses, traumatic brain injury, neoangiogenesis, Endothelial monocyte-activating polypeptide, progenitor cell, oligodendrocyte, Multipotent, traumatic injuries
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