MiR-29a Knockout Aggravates Neurological Damage by Pre-polarizing M1 Microglia in Experimental Rat Models of Acute Stroke.
MiR-29a Knockout Aggravates Neurological Damage by Pre-polarizing M1 Microglia in Experimental Rat Models of Acute Stroke.
复制标题
在急性中风实验大鼠模型中，MiR-29a 敲除通过预极化 M1 小胶质细胞加重神经损伤
DOI：
10.3389/fgene.2021.642079
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发表时间：
2021
影响因子：
3.7
通讯作者：
Ma Y
中科院分区：
文献类型：
--
作者：
Zhao F;Zhao H;Fan J;Wang R;Han Z;Tao Z;Zheng Y;Yan F;Huang Y;Yu L;Zhang X;Qi X;Zhang L;Luo Y;Ma Y
目的探讨miR-29 a-5 p基因敲除对急性缺血性脑卒中后神经损伤的影响，加深对缺血后损伤分子机制的认识，为缺血性脑损伤的治疗提供新的思路。方法建立miR-29 a-5 p基因敲除大鼠和野生型SD大鼠大脑中动脉闭塞模型。采用实时荧光定量PCR检测缺血大鼠血浆、皮质、基底节、缺血性脑卒中患者血浆、中性粒细胞以及缺氧胶质细胞中miR-29 a的水平。TTC染色检测梗死体积，Western blotting检测星形胶质细胞和小胶质细胞的活化情况。结果MCAO模型大鼠血和脑组织中miR-29 a-5 p表达水平均降低。此外，急性脑卒中患者外周血中miR-29 a-5 p水平降低。miR-29 a敲除可增加MCAO大鼠模型的梗死体积，并且miR-29 a敲除显示MCAO大鼠脑中小胶质细胞的M1极化。MCAO后大鼠中的miR-29 a敲除促进星形胶质细胞增殖并增加谷氨酸释放。结论miR-29 a基因敲除可促进M1小胶质细胞极化，增加谷氨酸释放，从而加重实验性脑卒中大鼠模型的神经功能损害。
Objective By exploring the effects of miR-29a-5p knockout on neurological damage after acute ischemic stroke, we aim to deepen understanding of the molecular mechanisms of post-ischemic injury and thus provide new ideas for the treatment of ischemic brain injury. Methods miR-29a-5p knockout rats and wild-type SD rats were subjected to transient middle cerebral artery occlusion (MCAO). miR-29a levels in plasma, cortex, and basal ganglia of ischemic rats, and in plasma and neutrophils of ischemic stroke patients, as well as hypoxic glial cells were detected by real-time PCR. The infarct volume was detected by TTC staining and the activation of astrocytes and microglia was detected by western blotting. Results The expression of miR-29a-5p was decreased in parallel in blood and brain tissue of rat MCAO models. Besides, miR-29a-5p levels were reduced in the peripheral blood of acute stroke patients. Knockout of miR-29a enhanced infarct volume of the MCAO rat model, and miR-29a knockout showed M1 polarization of microglia in the MCAO rat brain. miR-29a knockout in rats after MCAO promoted astrocyte proliferation and increased glutamate release. Conclusion Knockout of miR-29a in rats promoted M1 microglial polarization and increased glutamate release, thereby aggravating neurological damage in experimental stroke rat models.
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影响因子：
56.9
作者：
Lagos-Quintana, M;Rauhut, R;Tuschl, T
通讯作者：
Tuschl, T
DOI：
10.1038/jcbfm.2008.157
发表时间：
2009-04
期刊：
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
影响因子：
--
作者：
通讯作者：
--
影响因子：
8.2
作者：
Kim JY;Bae HJ
通讯作者：
Bae HJ
缺血性中风患者循环免疫细胞中 Mir-424 水平升高的诊断和免疫抑制潜力。
影响因子：
7.4
作者：
Li G;Ma Q;Wang R;Fan Z;Tao Z;Liu P;Zhao H;Luo Y
通讯作者：
Luo Y
DOI：
10.1073/pnas.1111098109
发表时间：
2012-01-24
影响因子：
11.1
作者：
Pascual, Olivier;Ben Achour, Sarrah;Bessis, Alain
通讯作者：
Bessis, Alain