题名 | Genetic inactivation of the adenosine A2A receptor exacerbates brain damage in mice with experimental autoimmune encephalomyelitis |
作者 | |
发表日期 | 2012-10 |
发表期刊 | JOURNAL OF NEUROCHEMISTRY 影响因子和分区 |
语种 | 英语 |
原始文献类型 | Article |
关键词 | adenosine A1 receptors adenosine A2A receptors CD4+T cells experimental autoimmune encephalomyelitis (EAE) microglial cells multiple sclerosis |
其他关键词 | CD8(+) T-CELLS ; CENTRAL-NERVOUS-SYSTEM ; EMERGING THERAPEUTIC TARGETS ; MULTIPLE-SCLEROSIS ; A(2A) RECEPTORS ; SPINAL-CORD ; FOCAL ISCHEMIA ; MOUSE STRIATUM ; TISSUE-DAMAGE ; ADULT RATS |
摘要 | Studies with multiple sclerosis patients and animal models of experimental autoimmune encephalomyelitis (EAE) implicate adenosine and adenosine receptors in modulation of neuroinflammation and brain injury. Although the involvement of the A1 receptor has been recently demonstrated, the role of the adenosine A2A receptor (A2AR) in development of EAE pathology is largely unknown. Using mice with genetic inactivation of the A2A receptor, we provide direct evidence that loss of the A2AR exacerbates EAE pathology in mice. Compared with wild-type mice, A2AR knockout mice injected with myelin oligodendroglia glycoprotein peptide had a higher incidence of EAE and exhibited higher neurological deficit scores and greater decrease in body weight. A2AR knockout mice displayed increased inflammatory cell infiltration and enhanced microglial cell activation in cortex, brainstem, and spinal cord. In addition, demyelination and axonal damage in brainstem were exacerbated, levels of Th1 cytokines increased, and Th2 cytokines decreased. Collectively, these findings suggest that extracellular adenosine acting at A2ARs triggers an important neuroprotective mechanism. Thus, the A2A receptor is a potential target for therapeutic approaches to multiple sclerosis. |
资助项目 | Wenzhou Medical College Key Research Project [30328015]; Joint Found of China Ministry of Public Health-Zhejiang Bureau of Health [WKJ 2005-2-041]; Wenzhou Science &Technology bureau [H20100014]; Building Funding of Zhejiang Key Subject (Pharmacology and Biochemical Pharmaceutics); US public health grant [(NIH) NS41083]; NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKEUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Neurological Disorders & Stroke (NINDS) [R01NS041083] Funding Source: NIH RePORTER |
出版者 | WILEY-BLACKWELL |
出版地 | HOBOKEN |
ISSN | 0022-3042 |
EISSN | 1471-4159 |
卷号 | 123期号:1页码:100-112 |
DOI | 10.1111/j.1471-4159.2012.07807.x |
页数 | 13 |
WOS类目 | Biochemistry & Molecular Biology ; Neurosciences |
WOS研究方向 | Biochemistry & Molecular Biology ; Neurosciences & Neurology |
WOS记录号 | WOS:000308631800009 |
收录类别 | SCIE ; PUBMED ; SCOPUS |
URL | 查看原文 |
PubMed ID | 22639925 |
SCOPUSEID | 2-s2.0-84866251649 |
通讯作者地址 | [Chen, Jiang-Fan]Department of Neurology,Wenzhou Medical College,First Affiliated Hospital,China |
Scopus学科分类 | Biochemistry;Cellular and Molecular Neuroscience |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | https://kms.wmu.edu.cn/handle/3ETUA0LF/16843 |
专题 | 第二临床医学院、附属第二医院、育英儿童医院_神经病学 附属第一医院 药学院(分析测试中心)_实验神经生物研究所 |
通讯作者 | Chen, Jiang-Fan |
作者单位 | 1.Department of Neurology,Wenzhou Medical College,First Affiliated Hospital,China; 2.Department of Neurology,Boston University,School of Medicine,715 Albany Street, C329,United States |
第一作者单位 | 附属第一医院 |
通讯作者单位 | 附属第一医院 |
第一作者的第一单位 | 附属第一医院 |
推荐引用方式 GB/T 7714 | Yao, Shu-Qin,Li, Zheng-Zheng,Huang, Qing-Yuan,et al. Genetic inactivation of the adenosine A2A receptor exacerbates brain damage in mice with experimental autoimmune encephalomyelitis[J]. JOURNAL OF NEUROCHEMISTRY,2012,123(1):100-112. |
APA | Yao, Shu-Qin., Li, Zheng-Zheng., Huang, Qing-Yuan., Li, Fang., Wang, Zhao-Wei., ... & Zheng, Rong-Yuan. (2012). Genetic inactivation of the adenosine A2A receptor exacerbates brain damage in mice with experimental autoimmune encephalomyelitis. JOURNAL OF NEUROCHEMISTRY, 123(1), 100-112. |
MLA | Yao, Shu-Qin,et al."Genetic inactivation of the adenosine A2A receptor exacerbates brain damage in mice with experimental autoimmune encephalomyelitis".JOURNAL OF NEUROCHEMISTRY 123.1(2012):100-112. |
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