Abstract：
:Excessive 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.
journal_name
Neurosciencejournal_title
Neuroscienceauthors
Zhou Z,Gao S,Li Y,Peng R,Zheng Z,Wei W,Zhao Z,Liu X,Li L,Zhang Jdoi
10.1016/j.neuroscience.2020.04.042subject
Has Abstractpub_date
2020-07-01 00:00:00pages
60-69eissn
0306-4522issn
1873-7544pii
S0306-4522(20)30276-1journal_volume
438pub_type
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