title: Gene silencing of MCP-1 prevents microglial activation and inflammatory injury after intracerebral hemorrhage.
abstract: Microglia are activated after intracerebral hemorrhage and induce neuron death by releasing proinflammatory cytokines and chemokines. However, the related mechanism of microglia activation in such conditions remains elusive. MCP-1, the ligand of CCR2 expressed in the central nervous system, could promote microglia proliferation, survival and cytokine secretion. According to the previous findings, we make a hypothesis that whether alternation of MCP-1 level could attenuate microglia activation and toxicity to neuron in intracerebral hemorrhage. To identify that, we interfere with the MCP-1 expression of microglia by RNAi technology, and coculture the microglia and neuron in ICH. The results demonstrated that MCP-1 RNAi inhibited TNF-α, IL-1β and IL-6 expression in microglia and attenuated neuron injury. In conclusion, the present study suggests that MCP-1 might promote ICH induced microglia activation and toxicity to neuron, and MCP-1 RNAi might provide promising therapeutical strategy for ICH.
authors: Department of Neurology, Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
authors: Zhao
authors: Z
authors: Yang
authors: Department of Neurology, Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
authors: Juan
authors: J
authors: Wang
authors: Department of Orthopedics, Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
authors: Yu
authors: Y
authors: Yu
authors: Department of Neurology, Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China. Electronic address: lzw023@126.com.
authors: Zhiwei
authors: Z
authors: Li
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D002543:Cerebral Hemorrhage / Q000276:immunology / Q000628:therapy*; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism*; D018920:Coculture Techniques; D005786:Gene Expression Regulation / Q000235:genetics; D020868:Gene Silencing; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D017628:Microglia / Q000502:physiology*; D009474:Neurons / Q000502:physiology*; D034741:RNA, Small Interfering / Q000235:genetics / Q000627:therapeutic use*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D053583:Interleukin-1beta; D015850:Interleukin-6; D034741:RNA, Small Interfering; D014409:Tumor Necrosis Factor-alpha
keywords: Activation; ICH; Inflammation; MCP-1; Microglia