Complement C3 Aggravates Post-epileptic Neuronal Injury Via Activation of TRPV1.
10.1007/s12264-021-00750-4
- Author:
Guang-Tong JIANG
1
;
Lin SHAO
1
;
Shuo KONG
1
;
Meng-Liu ZENG
1
;
Jing-Jing CHENG
1
;
Tao-Xiang CHEN
1
;
Song HAN
2
;
Jun YIN
2
;
Wan-Hong LIU
3
;
Xiao-Hua HE
2
;
Yu-Min LIU
4
;
Lanzi GONGGA
5
;
Bi-Wen PENG
6
Author Information
1. Department of Physiology, Hubei Provincial Key Laboratory of Developmentally Originated Disease, School of Basic Medical Sciences, Wuhan University, Wuhan, 430071, China.
2. Department of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, 430071, China.
3. Department of Immunology, School of Basic Medical Sciences, Wuhan University, Wuhan, 430071, China.
4. Department of Neurology, Zhongnan Hospital, Wuhan University, Wuhan, 430071, China.
5. Medical College, Tibet University, Lhasa, 850013, China.
6. Department of Physiology, Hubei Provincial Key Laboratory of Developmentally Originated Disease, School of Basic Medical Sciences, Wuhan University, Wuhan, 430071, China. pengbiwen@whu.edu.cn.
- Publication Type:Journal Article
- Keywords:
CircRad52;
Cognitive disorder;
Complement C3;
Epilepsy;
TRPV1
- MeSH:
Animals;
Astrocytes/metabolism*;
Complement C3/metabolism*;
Epilepsy;
Mice;
Neurons/pathology*;
Status Epilepticus;
TRPV Cation Channels/metabolism*
- From:
Neuroscience Bulletin
2021;37(10):1427-1440
- CountryChina
- Language:English
-
Abstract:
Epilepsy is a brain condition characterized by the recurrence of unprovoked seizures. Recent studies have shown that complement component 3 (C3) aggravate the neuronal injury in epilepsy. And our previous studies revealed that TRPV1 (transient receptor potential vanilloid type 1) is involved in epilepsy. Whether complement C3 regulation of neuronal injury is related to the activation of TRPV1 during epilepsy is not fully understood. We found that in a mouse model of status epilepticus (SE), complement C3 derived from astrocytes was increased and aggravated neuronal injury, and that TRPV1-knockout rescued neurons from the injury induced by complement C3. Circular RNAs are abundant in the brain, and the reduction of circRad52 caused by complement C3 promoted the expression of TRPV1 and exacerbated neuronal injury. Mechanistically, disorders of neuron-glia interaction mediated by the C3-TRPV1 signaling pathway may be important for the induction of neuronal injury. This study provides support for the hypothesis that the C3-TRPV1 pathway is involved in the prevention and treatment of neuronal injury and cognitive disorders.
