mTORC1 pathway disruption ameliorates brain inflammation following stroke via a shift in microglia phenotype from M1 type to M2 type
文献类型：期刊论文
| 作者 | Li, Daojing1,2; Wang, Chunjiong3; Yao, Yang1,2; Chen, Li1,2; Liu, Guiyou5; Zhang, Rongxin4; Liu, Qiang1,2,6; Shi, Fu-Dong1,2,6; Hao, Junwei1,2 |
| 刊名 | FASEB JOURNAL
 |
| 出版日期 | 2016-10-01 |
| 卷号 | 30期号:10页码:3388-3399 |
| 关键词 | ischemia glia cells polarization |
| 英文摘要 | Inflammatory factors secreted by microglia play an important role in focal ischemic stroke. The mammalian target of rapamycin (mTOR) pathway is a known regulator of immune responses, but the role that mTORC1 signaling plays in poststroke neuroinflammation is not clear. To explore the relationship between microglial action in the mTORC1 pathway and the impact on stroke, we administered the mTORC1 inhibitors sirolimus and everolimus to mice. Presumably, disrupting the mTORC1 pathway after focal ischemic stroke should clarify the subsequent activity of microglia. For that purpose, we generated mice deficient in the regulatory associated protein of mTOR (Raptor) in microglia, whose mTORC1 signaling was blocked, by crossing Raptor loxed (Raptor(flox/flox)) mice with CX3CR1(CreER) mice, which express Cre recombinase under the control of the CX3C chemokine receptor 1 promoter. mTORC1 blockade reduced lesion size, improved motor function, dramatically decreased production of proinflammatory cytokines and chemokines, and reduced the number of M1 type microglia. Thus, mTORC1 blockade apparently attenuated behavioral deficits and poststroke inflammation after middle cerebral artery occlusion by preventing microglia polarization toward the M1 type. |
| WOS标题词 | Science & Technology ; Life Sciences & Biomedicine |
| 类目[WOS] | Biochemistry & Molecular Biology ; Biology ; Cell Biology |
| 研究领域[WOS] | Biochemistry & Molecular Biology ; Life Sciences & Biomedicine - Other Topics ; Cell Biology |
| 关键词[WOS] | FOCAL CEREBRAL-ISCHEMIA ; MICROGLIA/MACROPHAGE POLARIZATION ; MACROPHAGE POLARIZATION ; OXIDATIVE STRESS ; ARTERY OCCLUSION ; INJURY ; RAPAMYCIN ; CELLS ; ACTIVATION ; EVEROLIMUS |
| 收录类别 | SCI |
| 语种 | 英语 |
| WOS记录号 | WOS:000384329800011 |
| 源URL | [http://124.16.173.210/handle/834782/2934]  |
| 专题 | 天津工业生物技术研究所_基因组分析实验室 陈祖耕_期刊论文 |
| 作者单位 | 1.Tianjin Med Univ, Gen Hosp, Dept Neurol, Tianjin 300052, Peoples R China 2.Tianjin Med Univ, Gen Hosp, Tianjin Neurol Inst, Tianjin 300052, Peoples R China 3.Tianjin Med Univ, Dept Physiol & Pathophysiol, Tianjin, Peoples R China 4.Tianjin Med Univ, Dept Immunol, Tianjin, Peoples R China 5.Chinese Acad Sci, Tianjin Inst Ind Biotechnol, Tianjin, Peoples R China 6.St Josephs Hosp, Barrow Neurol Inst, Dept Neurol, Phoenix, AZ USA |
| 推荐引用方式 GB/T 7714 | Li, Daojing,Wang, Chunjiong,Yao, Yang,et al. mTORC1 pathway disruption ameliorates brain inflammation following stroke via a shift in microglia phenotype from M1 type to M2 type[J]. FASEB JOURNAL,2016,30(10):3388-3399. |
| APA | Li, Daojing.,Wang, Chunjiong.,Yao, Yang.,Chen, Li.,Liu, Guiyou.,...&Hao, Junwei.(2016).mTORC1 pathway disruption ameliorates brain inflammation following stroke via a shift in microglia phenotype from M1 type to M2 type.FASEB JOURNAL,30(10),3388-3399. |
| MLA | Li, Daojing,et al."mTORC1 pathway disruption ameliorates brain inflammation following stroke via a shift in microglia phenotype from M1 type to M2 type".FASEB JOURNAL 30.10(2016):3388-3399. |
入库方式： OAI收割
来源：天津工业生物技术研究所
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