Endothelial tyrosine kinase receptor B prevents VE-cadherin cleavage and protects against atherosclerotic lesion development in ApoE−/− mice

Hong Jiang; Shuhong Huang; Xinyun Li; Xian Li; Shanying Huang; Yun Zhang; Zhe-Yu Chen

doi:10.18632/oncotarget.5855

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Research Papers: Pathology:

Endothelial tyrosine kinase receptor B prevents VE-cadherin cleavage and protects against atherosclerotic lesion development in ApoE−/− mice

Hong Jiang, Shuhong Huang, Xinyun Li, Xian Li, Shanying Huang, Yun Zhang and Zhe-Yu Chen _

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Oncotarget. 2015; 6:30640-30649. https://doi.org/10.18632/oncotarget.5855

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Abstract

Hong Jiang1, Shuhong Huang2, Xinyun Li1, Xian Li2, Shanying Huang1, Yun Zhang1 and Zhe-Yu Chen2

1 Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Qilu Hospital, Shandong University, Jinan, Shandong, China

2 Department of Neurobiology, Shandong Provincial Key Laboratory of Mental Disorders, School of Medicine, Shandong University, Jinan, Shandong, China

Correspondence to:

Zhe-Yu Chen, email:

Yun Zhang, email:

Keywords: atherosclerosis, endothelial barrier dysfunction, brain-derived neurotrophic factor, tyrosine kinase receptor B, vascular endothelial cadherin, Pathology Section

Received: June 30, 2015 Accepted: September 06, 2015 Published: September 28, 2015

Abstract

Tyrosine kinase receptor B (TrkB) is a high-affinity receptor for brain-derived neurotrophic factor (BDNF). In addition to its nervous system functions, TrkB is also expressed in the aortic endothelium. However, the effects of endothelial TrkB signaling on atherosclerosis remained unknown. Immunofluorescence analysis revealed that TrkB expression is downregulated in the endothelium of atherosclerotic lesions from ApoE-/- mice compared with the atheroma-free aorta of WT mice. Endothelial TrkB knockdown led to increased lesion size, lipid deposition and inflammatory responses in the atherosclerotic lesions of the ApoE-/- mice compared with the control mice. Mechanistic studies showed that TrkB activation prevented VE-cadherin shedding by enhancing the interaction between vascular endothelial protein tyrosine phosphatase and VE-cadherin, maintaining VE-cadherin in a dephosphorylated state. Our data demonstrate that TrkB is an endothelial injury-response molecule in atherogenesis. Endothelial BDNF/TrkB signaling reduces VE-cadherin shedding and protects against atherosclerotic lesion development in ApoE−/− mice.

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Research Papers: Pathology:

Endothelial tyrosine kinase receptor B prevents VE-cadherin cleavage and protects against atherosclerotic lesion development in ApoE−/− mice

Abstract