EphrinB2 activation enhances angiogenesis, reduces amyloid-β deposits and secondary damage in thalamus at the early stage after cortical infarction in hypertensive rats

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http://journals.sagepub.com/doi/abs/10.1177/0271678X18769188

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Shihui Xing¹

Shihui Xing

1Department of Neurology and Stroke Center, 71068The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China
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, Nannan Pan²

Nannan Pan

2Department of Neurology, The Affiliated Brain Hospital of Guangzhou Medical University, Guangzhou, China
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, Wei Xu¹

Wei Xu

1Department of Neurology and Stroke Center, 71068The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China
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Jian Zhang¹

Jian Zhang

1Department of Neurology and Stroke Center, 71068The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China
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, Jingjing Li¹

Jingjing Li

1Department of Neurology and Stroke Center, 71068The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China
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, Chao Dang¹

Chao Dang

1Department of Neurology and Stroke Center, 71068The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China
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, Gang Liu¹

Gang Liu

1Department of Neurology and Stroke Center, 71068The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China
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, Zhong Pei¹

Zhong Pei

1Department of Neurology and Stroke Center, 71068The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China
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, Jinsheng Zeng¹

Jinsheng Zeng

1Department of Neurology and Stroke Center, 71068The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China
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First Published April 6, 2018 Research Article

https://doi.org/10.1177/0271678X18769188

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Article Information

Article first published online: April 6, 2018
Received: November 04, 2017; Accepted: March 14, 2018

https://doi.org/10.1177/0271678X18769188

Shihui Xing¹, Nannan Pan², Wei Xu¹, Jian Zhang¹, Jingjing Li¹, Chao Dang¹, Gang Liu¹, Zhong Pei¹, Jinsheng Zeng¹

¹Department of Neurology and Stroke Center, 71068The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China

²Department of Neurology, The Affiliated Brain Hospital of Guangzhou Medical University, Guangzhou, China

Corresponding Author: Shihui Xing and Jinsheng Zeng, Stroke Center and Department of Neurology, The First Affiliated Hospital, Sun Yat-Sen University, No. 58 Zhongshan Road 2, Guangzhou 510080, China. Email: xingshih@mail.sysu.edu.cn; zengjs@pub.guangzhou.gd.cn

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Abstract

Cerebral infarction causes secondary neurodegeneration and angiogenesis in thalamus, which impacts functional recovery after stroke. Here, we hypothesize that activation of ephrinB2 could stimulate angiogenesis and restore the secondary neurodegeneration in thalamus after cerebral infarction. Focal cerebral infarction was induced by middle cerebral artery occlusion (MCAO). Secondary damage, angiogenesis, amyloid-β (Aβ) deposits, levels of ephrinB2 and receptor for advanced glycation end product (RAGE) in the ipsilateral thalamus were determined by immunofluorescence and immunoblot. The contribution of ephrinB2 to angiogenesis was determined by siRNA-mediated knockdown of ephrinB2 and pharmacological activation of ephrinB2. The results showed that formation of new vessels and ephrinB2 expression was markedly increased in the ipsilateral thalamus at seven days after MCAO. EphrinB2 knockdown markedly suppressed angiogenesis coinciding with increased Aβ accumulation, neuronal loss and gliosis in the ipsilateral thalamus. In contrast, clustered EphB2-Fc significantly enhanced angiogenesis, alleviated Aβ accumulation and the secondary thalamic damage, which was accompanied by accelerated function recovery. Additionally, activation of ephrinB2 significantly reduced RAGE levels in the ipsilateral thalamus. Our findings suggest that activation of ephrinB2 promotes angiogenesis, ameliorates Aβ accumulation and the secondary thalamic damage after cerebral infarction. Additionally, RAGE might be involved in Aβ clearance by activating ephrinB2 in the thalamus.