Cerebral Ischemia Is Exacerbated by Extracellular Nicotinamide Phosphoribosyltransferase via a Non-Enzymatic Mechanism.docVIP
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Cerebral Ischemia Is Exacerbated by Extracellular Nicotinamide Phosphoribosyltransferase via a Non-Enzymatic Mechanism
Cerebral Ischemia Is Exacerbated by Extracellular
Nicotinamide Phosphoribosyltransferase via a Non-
Enzymatic Mechanism
Bing Zhao1,4?, Meng Zhang3?, Xue Han1 1 2 2 1
, Xia-Yan Zhang , Qiong Xing , Xu Dong , Qiao-Juan Shi , Peng
Huang
, Yun-Bi Lu , Er-Qing Wei , Qiang Xia , Wei-Ping Zhang , Chun Tang
1 1 1 3 1* 2
1 Department of Pharmacology, Key Laboratory of Medical Neurobiology of Ministry of Health of China, Zhejiang Province Key Laboratory of Neurobiology,
Zhejiang University School of Medicine, Hangzhou, Zhejiang, China, 2 State Key Laboratory of Magnetic Resonance and Atomic and Molecular Physics, Wuhan
Center for Magnetic, Wuhan Institute of Physics and Mathematics, Chinese Academy of Sciences, Wuhan, China, 3 Department of Physiology, Zhejiang
University School of Medicine, Hangzhou, China, 4 Department of Anesthesiology, the First Affiliated Hospital, School of Medicine, Zhejiang University,
Hangzhou, China
Abstract
Intracellular nicotinamide phosphoribosyltransferase (iNAMPT) in neuron has been known as a protective factor
against cerebral ischemia through its enzymatic activity, but the role of central extracellular NAMPT (eNAMPT) is not
clear. Here we show that eNAMPT protein level was elevated in the ischemic rat brain after middle-cerebral-artery
occlusion (MCAO) and reperfusion, which can be traced to at least in part from blood circulation. Administration of
recombinant NAMPT protein exacerbated MCAO-induced neuronal injury in rat brain, while exacerbated oxygen-
glucose-deprivation (OGD) induced neuronal injury only in neuron-glial mixed culture, but not in
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