Multiple Mild Stimulations Reduce Membrane Distribution of CX3CR1 Promoted by Annexin a1 in Microglia to Attenuate Excessive Dendritic Spine Pruning and Cognitive Deficits Caused by a Transient Ischemic Attack in Mice.
10.1007/s12264-022-00847-4
- Author:
Lu ZHENG
1
;
Yi WANG
1
;
Bin SHAO
1
;
Huijuan ZHOU
1
;
Xing LI
1
;
Cai ZHANG
2
;
Ning SUN
3
;
Jing SHI
4
Author Information
1. Department of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
2. Department of Clinical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
3. Department of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. nsun@hust.edu.cn.
4. Department of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. sj@mails.tjmu.edu.cn.
- Publication Type:Journal Article
- Keywords:
Annexin a1;
CX3CR1;
Dendritic spine pruning;
Microglia;
Multiple mild stimulations;
Transient ischemic attack
- MeSH:
Animals;
Annexin A1/metabolism*;
CX3C Chemokine Receptor 1/metabolism*;
Chemokine CX3CL1;
Cognition;
Dendritic Spines/metabolism*;
Ischemic Attack, Transient;
Mice;
Microglia/metabolism*
- From:
Neuroscience Bulletin
2022;38(7):753-768
- CountryChina
- Language:English
-
Abstract:
A transient ischemic attack (TIA) can cause reversible and delayed impairment of cognition, but the specific mechanisms are still unclear. Annexin a1 (ANXA1) is a phospholipid-binding protein. Here, we confirmed that cognition and hippocampal synapses were impaired in TIA-treated mice, and this could be rescued by multiple mild stimulations (MMS). TIA promoted the interaction of ANXA1 and CX3CR1, increased the membrane distribution of CX3CR1 in microglia, and thus enhanced the CX3CR1 and CX3CL1 interaction. These phenomena induced by TIA could be reversed by MMS. Meanwhile, the CX3CR1 membrane distribution and CX3CR1-CX3CL1 interaction were upregulated in primary cultured microglia overexpressing ANXA1, and the spine density was significantly reduced in co-cultured microglia overexpressing ANXA1 and neurons. Moreover, ANXA1 overexpression in microglia abolished the protection of MMS after TIA. Collectively, our study provides a potential strategy for treating the delayed synaptic injury caused by TIA.
