Regulation of endothelial intracellular adenosine via adenosine kinase epigenetically modulates vascular inflammation

Yiming Xu (), Yong Wang, Siyuan Yan, Qiuhua Yang, Yaqi Zhou, Xianqiu Zeng, Zhiping Liu, Xiaofei An, Haroldo A. Toque, Zheng Dong, Xuejun Jiang, David J. Fulton, Neal L. Weintraub, Qinkai Li, Zsolt Bagi, Mei Hong, Detlev Boison, Chaodong Wu and Yuqing Huo ()
Additional contact information
Yiming Xu: Augusta University
Yong Wang: Augusta University
Siyuan Yan: Augusta University
Qiuhua Yang: Augusta University
Yaqi Zhou: Augusta University
Xianqiu Zeng: Augusta University
Zhiping Liu: Augusta University
Xiaofei An: Augusta University
Haroldo A. Toque: Augusta University
Zheng Dong: Medical College of Georgia, Augusta University
Xuejun Jiang: Chinese Academy of Science
David J. Fulton: Augusta University
Neal L. Weintraub: Augusta University
Qinkai Li: Peking University Shenzhen Graduate School
Zsolt Bagi: Augusta University
Mei Hong: Peking University Shenzhen Graduate School
Detlev Boison: Legacy Research Institute
Chaodong Wu: Texas A&M University
Yuqing Huo: Augusta University

Nature Communications, 2017, vol. 8, issue 1, 1-16

Abstract: Abstract The molecular mechanisms underlying vascular inflammation and associated inflammatory vascular diseases are not well defined. Here we show that endothelial intracellular adenosine and its key regulator adenosine kinase (ADK) play important roles in vascular inflammation. Pro-inflammatory stimuli lead to endothelial inflammation by increasing endothelial ADK expression, reducing the level of intracellular adenosine in endothelial cells, and activating the transmethylation pathway through increasing the association of ADK with S-adenosylhomocysteine (SAH) hydrolase (SAHH). Increasing intracellular adenosine by genetic ADK knockdown or exogenous adenosine reduces activation of the transmethylation pathway and attenuates the endothelial inflammatory response. In addition, loss of endothelial ADK in mice leads to reduced atherosclerosis and affords protection against ischemia/reperfusion injury of the cerebral cortex. Taken together, these results demonstrate that intracellular adenosine, which is controlled by the key molecular regulator ADK, influences endothelial inflammation and vascular inflammatory diseases.

Date: 2017
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DOI: 10.1038/s41467-017-00986-7

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