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Fractalkine/CX3CR1 axis is critical for neuroprotection induced by hypoxic postconditioning against cerebral ischemic injury.
Zhan, Lixuan; Qiu, Meiqian; Zheng, Jianhua; Lai, Meijing; Lin, Kunqin; Dai, Jiahua; Sun, Weiwen; Xu, En.
Afiliação
  • Zhan L; Department of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, 250 Changgang Dong RD, Guangzhou, 510260, P. R. China.
  • Qiu M; Department of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, 250 Changgang Dong RD, Guangzhou, 510260, P. R. China.
  • Zheng J; Department of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, 250 Changgang Dong RD, Guangzhou, 510260, P. R. China.
  • Lai M; Department of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, 250 Changgang Dong RD, Guangzhou, 510260, P. R. China.
  • Lin K; Department of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, 250 Changgang Dong RD, Guangzhou, 510260, P. R. China.
  • Dai J; Department of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, 250 Changgang Dong RD, Guangzhou, 510260, P. R. China.
  • Sun W; Department of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, 250 Changgang Dong RD, Guangzhou, 510260, P. R. China.
  • Xu E; Department of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, 250 Changgang Dong RD, Guangzhou, 510260, P. R. China. enxu@163.net.
Cell Commun Signal ; 22(1): 457, 2024 Sep 26.
Article em En | MEDLINE | ID: mdl-39327578
ABSTRACT
Microglial activation-mediated neuroinflammation is a major contributor to neuronal damage after cerebral ischemia. The Fractalkine (FKN)/CX3C chemokine receptor 1 (CX3CR1) axis plays a critical role in regulating microglial activation and neuroinflammation. The aim of this study is to ascertain the role and mechanism of FKN/CX3CR1 axis in hypoxic postconditioning (HPC)-induced anti-inflammatory and neuroprotective effects on transient global cerebral ischemia (tGCI). We found that HPC suppressed microglial activation and alleviated neuroinflammation in hippocampal CA1 after tGCI. Meanwhile, HPC upregulated the expression of FKN and CX3CR1 in neurons, but it downregulated the expression of CX3CR1 in glial cells after tGCI. In addition, the overexpression of FKN induced by the administration of FKN-carried lentivirus reduced microglial activation and inhibited neuroinflammation in CA1 after tGCI. Furthermore, silencing CX3CR1 with CX3CRi-carried lentivirus in CA1 after tGCI suppressed microglial activation and neuroinflammation and exerted neuroprotective effects. Finally, the overexpression of FKN caused a marked increase of neuronal CX3CR1 receptors, upregulated the phosphorylation of Akt, and reduced neuronal loss of rats in CA1 after tGCI. These findings demonstrated that HPC protected against neuronal damage in CA1 of tGCI rats through inhibiting microglial activation and activating Akt signaling pathway via FKN/CX3CR1 axis.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Microglia / Quimiocina CX3CL1 / Neuroproteção / Receptor 1 de Quimiocina CX3C Limite: Animals Idioma: En Revista: Cell Commun Signal Ano de publicação: 2024 Tipo de documento: Article País de publicação: Reino Unido
Texto completo
Adicionar na Minha BVS
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XML
PubMed Links
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Microglia / Quimiocina CX3CL1 / Neuroproteção / Receptor 1 de Quimiocina CX3C Limite: Animals Idioma: En Revista: Cell Commun Signal Ano de publicação: 2024 Tipo de documento: Article País de publicação: Reino Unido