机构：[1]Department of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China昆明医科大学附属第一医院[2]Department of Neurology, Barrow Neurological Institute, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, USA[3]Department of Radiology, Barrow Neurological Institute, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, USA[4]Brown University Warren Alpert Medical School, Providence, RI, USA.
The chemokine fractalkine (CX3CL1) and its receptor CX3CR1 play a fundamental role in the pathophysiology of stroke. Previous studies have focused on a paracrine interaction between neurons that produce fractalkine and microglia that express CX3CR1 receptors in the central nervous system. Recent findings have demonstrated the functional expression of CX3CR1 receptors by hippocampal neurons, suggesting their involvement in neuroprotective and neurodegenerative actions. To elucidate the roles of neuronal CX3CR1 in CX3CR1 levels, apoptosis-associated morphological changes, and Caspase 3-positive neuronal cells were observed in the striatum and in the hippocampus 24 hours after occlusion. Upregulation of CX3CR1 in ischemic neurons is associated with neuronal apoptotic cell death. In contrast, ischemia-induced apoptotic neuronal cell death was decreased in CX3CR1 deficient mice. Cultured primary hippocampal neurons obtained from CX3CR1 deficient mice were more resistant to glutamate-induced CXCR1 mediates neuronal apoptotic cell death in ischemia. Our results suggest that modulating CXCR1 activity offers a novel therapeutic strategy for stroke.
基金：
National Natural Science Foundation of ChinaNational Natural Science Foundation of China [81360204, 81760220]; Research Foundation of the First Affiliated Hospital of Kunming Medical University [2013BS08]; Yunnan Applied Basic Research Projects [2017FE467-135, 2017FB111, 2017NS057, 2016NS058, 2014NS178]
第一作者机构：[1]Department of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China
共同第一作者：
通讯作者：
通讯机构：[1]Department of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China[2]Department of Neurology, Barrow Neurological Institute, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, USA
推荐引用方式(GB/T 7714)：
Wang Jinkun,Gan Yan,Han Pengcheng,et al.Ischemia-induced Neuronal Cell Death Is Mediated by Chemokine Receptor CX3CR1[J].SCIENTIFIC REPORTS.2018,8:doi:10.1038/s41598-017-18774-0.
APA：
Wang, Jinkun,Gan, Yan,Han, Pengcheng,Yin, Junxiang,Liu, Qingwei...&Tang, Zhiwei.(2018).Ischemia-induced Neuronal Cell Death Is Mediated by Chemokine Receptor CX3CR1.SCIENTIFIC REPORTS,8,
MLA：
Wang, Jinkun,et al."Ischemia-induced Neuronal Cell Death Is Mediated by Chemokine Receptor CX3CR1".SCIENTIFIC REPORTS 8.(2018)
