Artery Research

Volume 23, Issue C, September 2018, Pages 45 - 51

The decrease of Tie-2 receptor phosphorylation in microvascular endothelial cells is involved in early brain injury after subarachnoid hemorrhage

Authors
Hua Gu, Yi-qi Wang*, Chao-Hui Zhao, Xing-ming Zhong, Jian-guo Yang
Department of Neurosurgery, The First People’s Hospital of Huzhou, The First Affiliated Hospital of Huzhou Teachers College, No. 158 Guangchanghou Road, Huzhou, Zhejiang Province, China
*Corresponding author. Fax:+86 05722039316. E-mail address: neruosurgeryhzyy@163.com (Y.-q. Wang).
Corresponding Author
Yi-qi Wang
Received 28 June 2018, Revised 24 July 2018, Accepted 31 July 2018, Available Online 23 August 2018.
DOI
https://doi.org/10.1016/j.artres.2018.07.004How to use a DOI?
Keywords
Tie-2 receptor, Microvascular endothelial cells, Early brain injury, Subarachnoid hemorrhage, Tight junction
Abstract

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.

Copyright
© 2018 Association for Research into Arterial Structure and Physiology. Published by Elsevier B.V. All rights reserved.
Open Access
This is an open access article distributed under the CC BY-NC license.

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Journal
Artery Research
Volume-Issue
23 - C
Pages
45 - 51
Publication Date
2018/08
ISSN (Online)
1876-4401
ISSN (Print)
1872-9312
DOI
https://doi.org/10.1016/j.artres.2018.07.004How to use a DOI?
Copyright
© 2018 Association for Research into Arterial Structure and Physiology. Published by Elsevier B.V. All rights reserved.
Open Access
This is an open access article distributed under the CC BY-NC license.

Cite this article

TY  - JOUR
AU  - Hua Gu
AU  - Yi-qi Wang
AU  - Chao-Hui Zhao
AU  - Xing-ming Zhong
AU  - Jian-guo Yang
PY  - 2018
DA  - 2018/08
TI  - The decrease of Tie-2 receptor phosphorylation in microvascular endothelial cells is involved in early brain injury after subarachnoid hemorrhage
JO  - Artery Research
SP  - 45
EP  - 51
VL  - 23
IS  - C
SN  - 1876-4401
UR  - https://doi.org/10.1016/j.artres.2018.07.004
DO  - https://doi.org/10.1016/j.artres.2018.07.004
ID  - Gu2018
ER  -