Neuroinflammation Mediates Faster Brachial Plexus Regeneration in Subjects with Cerebral Injury.
10.1007/s12264-021-00769-7
- Author:
Fan SU
1
;
Guobao WANG
1
;
Tie LI
1
;
Su JIANG
1
;
Aiping YU
1
;
Xiaomin WANG
2
;
Wendong XU
3
Author Information
1. Department of Hand Surgery, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, 200040, China.
2. Department of Hand and Upper Extremity Surgery, Jing'an District Central Hospital, Fudan University, Shanghai, 200040, China.
3. Department of Hand Surgery, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, 200040, China. wendongxu@fudan.edu.cn.
- Publication Type:Journal Article
- Keywords:
Brachial plexus injury;
Cerebral injury;
Contralateral seventh cervical nerve transfer;
Macrophage polarization;
Nerve regeneration;
Nerve transfer;
Neuroinflammation
- MeSH:
Animals;
Brachial Plexus;
Brachial Plexus Neuropathies/surgery*;
Humans;
Mice;
Nerve Transfer;
Peripheral Nerves;
Spinal Nerves
- From:
Neuroscience Bulletin
2021;37(11):1542-1554
- CountryChina
- Language:English
-
Abstract:
Our previous investigation suggested that faster seventh cervical nerve (C7) regeneration occurs in patients with cerebral injury undergoing contralateral C7 transfer. This finding needed further verification, and the mechanism remained largely unknown. Here, Tinel's test revealed faster C7 regeneration in patients with cerebral injury, which was further confirmed in mice by electrophysiological recordings and histological analysis. Furthermore, we identified an altered systemic inflammatory response that led to the transformation of macrophage polarization as a mechanism underlying the increased nerve regeneration in patients with cerebral injury. In mice, we showed that, as a contributing factor, serum amyloid protein A1 (SAA1) promoted C7 regeneration and interfered with macrophage polarization in vivo. Our results indicate that altered inflammation promotes the regenerative capacity of the C7 nerve by altering macrophage behavior. SAA1 may be a therapeutic target to improve the recovery of injured peripheral nerves.
