首页|The decrease of Tie-2 receptor phosphorylation in micro vascular endothelial cells is involved in early brain injury after subarachnoid hemorrhage
The decrease of Tie-2 receptor phosphorylation in micro vascular endothelial cells is involved in early brain injury after subarachnoid hemorrhage
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NSTL
Purpose: Loose endothelial cells and the destruction of the blood-brain barrier (BBB) are one of the pathophysiological mechanisms of early brain injury (EBI) after subarachnoid hemorrhage (SAH). Tie-2 receptor phosphorylation is important for maintaining integrity of microvascular endothelial cells and BBB. This study aimed to explore the role and changes of Tie-2 receptor phosphorylation levels in EBI after SAH.Methods: This study used an endovascular puncture model of rat to simulate the occurrence and development of aneurysmal subarachnoid hemorrhage. The location of Tie-2 receptor in brain tissues was determined by immunofluorescence. Immunofluorescence and western blot was carried out to observe the expression of Claudin-5 and Occludin in cortex and hippocampus. We chose to observe the Tie-2 receptor phosphorylation level in hippocampus according western blot. Evans blue viability assay was used to evaluate BBB permeability. Results: The results suggested that Tie-2 receptor mainly expressed around the vascular endothelial cells in brain. Following SAH, the Tie-2 receptor phosphorylation level and expression of tight junction protein (claudin-5 and occluding) decreased. Both of these downtrends were reversed by exogenous Angiopoietin-1 (Ang-1). Finally, injection of exogenous Ang-1 reduced SAH-associated BBB leakage.Conclusions: Our study indicated that Tie-2 receptor phosphorylation in microvascular endothelial cells was involved in pathophysiological process after SAH, and the decline of Tie-2 receptor phosphorylation might increase blood-brain barrier permeability by decreasing the tight junction protein expression.
NSTL
