• Ziwei Zhou, Shan Gao, Yadan Li, Ruilong Peng, Zhitong Zheng, Wei Wei, Zilong Zhao, Xilei Liu, Luyuan Li, and Jianning Zhang.
• Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, China; Tianjin Neurological Institute, Tianjin, China; Key Laboratory of Post-trauma Neuro-repair and Regeneration in Central Nervous System, Ministry of Education, Tianjin, China; Tianjin Key Laboratory of Injuries, Variations and Regeneration of Nervous System, Tianjin, China.
• Neuroscience. 2020 Jul 1; 438: 60-69.

AbstractExcessive expression of vascular endothelial growth factor (VEGF) is a common cause of blood-brain barrier (BBB) breakdown that triggers severe complications following traumatic brain injury (TBI). It has been shown that inhibition of VEGF activities may attenuate cerebral edema in pathological conditions. Vascular endothelial growth inhibitor (VEGI; also known as TNFSF15), a cytokine produced largely by vascular endothelial cells, is capable of downregulating VEGF expression and inhibiting VEGF receptor-2 (VEGFR2) activation. In this study we found that TBI can cause breakdown of BBB and sharp increases of VEGF/VEGI and Angpt2/Angpt1 ratios in the injured tissues. VEGI treatment resulted in a marked decrease of BBB permeability and concomitant restoration of normal ratios of VEGF/VEGI and Angpt2/Angpt1. Consistently, alleviated edema, decreased neuron cell death, and improved neurological functions were observed when the experimental animals were treated with VEGI in the early phase of TBI. Our findings suggest that administration of VEGI recombinant protein at early phases of TBI is beneficial to stabilization of the disease conditions.Copyright © 2020. Published by Elsevier Ltd.

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