当前位置:
X-MOL 学术
›
Brain Res. Bull.
›
论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
MST4 modulates the neuro-inflammatory response by regulating IκBα signaling pathway and affects the early outcome of experimental ischemic stroke in mice.
Brain Research Bulletin ( IF 3.8 ) Pub Date : 2019-11-10 , DOI: 10.1016/j.brainresbull.2019.10.011 Di Luan 1 , Yuanxiang Zhang 2 , Lili Yuan 1 , Zhaohu Chu 1 , Lingsong Ma 1 , Yang Xu 1 , Shoucai Zhao 1
Brain Research Bulletin ( IF 3.8 ) Pub Date : 2019-11-10 , DOI: 10.1016/j.brainresbull.2019.10.011 Di Luan 1 , Yuanxiang Zhang 2 , Lili Yuan 1 , Zhaohu Chu 1 , Lingsong Ma 1 , Yang Xu 1 , Shoucai Zhao 1
Affiliation
MST4 limits peripheral, macrophage-dependent inflammatory responses through direct phosphorylation of the adaptor TRAF6; though its role in neuro-inflammation is unclear. We investigated microglia expression of MST4 and whether is attenuates neuro-inflammatory response after cerebral ischemia-reperfusion injury in mice. Adult male C57BL6 mice were subjected to a 90-minute middle cerebral artery occlusion (MCAO) followed by a 72 -h reperfusing. The results showed that MST4 was involved in the pathological process after cerebral ischemia-reperfusion and was expressed in microglia. MST4-Adeno Associated Virus attenuated brain damage after MCAO and reduced expression of p-IκBα, p-ERK and p-JNK, while MST4 shRNA aggravated brain damage after MCAO and increased expression of p-IκBα, p-ERK and p-JNK. Our results show that MST4 inhibits neuro-inflammatory response in cerebral ischemia-reperfusion injury, improves neurological deficits, and reduces cerebral infarction volume in mice. Strategies to enhance MST4 in response to ischemic stroke may be a potential therapeutic strategy.
中文翻译:
MST4通过调节IκBα信号通路来调节神经炎症反应,并影响小鼠实验性缺血性卒中的早期结果。
MST4通过衔接子TRAF6的直接磷酸化限制外周巨噬细胞依赖性炎症反应。尽管其在神经炎症中的作用尚不清楚。我们调查了MST4的小胶质细胞表达,以及是否减轻了小鼠脑缺血再灌注损伤后的神经炎症反应。对成年雄性C57BL6小鼠进行90分钟的大脑中动脉闭塞(MCAO),然后进行72小时的再灌注。结果表明,MST4参与脑缺血再灌注后的病理过程,并在小胶质细胞中表达。MST4腺伴随病毒减轻MCAO后的脑损伤并降低p-IκBα,p-ERK和p-JNK的表达,而MST4 shRNA加重MCAO后的脑损伤并增加p-IκBα,p-ERK和p-JNK的表达。我们的结果表明,MST4抑制了小鼠脑缺血再灌注损伤中的神经炎症反应,改善了神经功能缺损,并减少了小鼠的脑梗死体积。响应缺血性卒中而增强MST4的策略可能是潜在的治疗策略。
更新日期:2019-11-10
中文翻译:
MST4通过调节IκBα信号通路来调节神经炎症反应,并影响小鼠实验性缺血性卒中的早期结果。
MST4通过衔接子TRAF6的直接磷酸化限制外周巨噬细胞依赖性炎症反应。尽管其在神经炎症中的作用尚不清楚。我们调查了MST4的小胶质细胞表达,以及是否减轻了小鼠脑缺血再灌注损伤后的神经炎症反应。对成年雄性C57BL6小鼠进行90分钟的大脑中动脉闭塞(MCAO),然后进行72小时的再灌注。结果表明,MST4参与脑缺血再灌注后的病理过程,并在小胶质细胞中表达。MST4腺伴随病毒减轻MCAO后的脑损伤并降低p-IκBα,p-ERK和p-JNK的表达,而MST4 shRNA加重MCAO后的脑损伤并增加p-IκBα,p-ERK和p-JNK的表达。我们的结果表明,MST4抑制了小鼠脑缺血再灌注损伤中的神经炎症反应,改善了神经功能缺损,并减少了小鼠的脑梗死体积。响应缺血性卒中而增强MST4的策略可能是潜在的治疗策略。