Brachial Plexus Root Avulsion Injury-Induced Endothelin-Converting Enzyme-Like 1 Overexpression Is Associated with Injured Motor Neurons Survival

Brachial plexus root avulsion (BPRA) injury arises from challenging delivery during childbirth, sports-related incidents, or car accidents, leading to extensive loss of motor neurons (MNs) and subsequent paralysis, including both motor and sensory impairment. Surgical nerve re-implantation cannot ef...

Full description

Saved in:
Bibliographic Details
Published in:Molecular neurobiology 2024-08, Vol.61 (8), p.5194-5205
Main Authors: Huang, Yu, Mai, Yunlin, Ye, Weijian, Lv, Shiqin, Zhou, Yingying, Wu, Pingzhen, Zhou, Lihua, Li, Yingqin, Zhong, Ke
Format: Article
Language:English
Subjects:
Activating transcription factor 3
AKT protein
Biomedical and Life Sciences
Biomedicine
Brachial plexus
c-Jun protein
Cell Biology
Endothelins
Enzymes
Injuries
Metalloproteinase
Motor neurons
Muscles
Neurobiology
Neurology
Neurosciences
Optic nerve
Paralysis
Recovery of function
Regeneration
Sciatic nerve
Sensory neurons
Transcription factors
TrkA protein
TrkA receptors
Citations: Items that this one cites
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Brachial plexus root avulsion (BPRA) injury arises from challenging delivery during childbirth, sports-related incidents, or car accidents, leading to extensive loss of motor neurons (MNs) and subsequent paralysis, including both motor and sensory impairment. Surgical nerve re-implantation cannot effectively restore motor function, and the survival of injured MNs is vital for axon regeneration and re-innervating the target muscles. Therefore, identifying novel molecular targets to improve injured MNs survival is of great significance in the treatment of BPRA injuries. Endothelin-converting enzyme-like 1 (ECEL1), a membrane-bound metallopeptidase, was initially identified as a molecule associated with nerve injuries. Damaged neurons exhibit a significant increase in the expression of ECEL1 following various types of nerve injuries, such as optic nerve injury and sciatic nerve injury. This study aimed to investigate the relationship between ECEL1 overexpression and the survival of injured MNs following BPRA injury. Our results observed a significant elevation in ECEL1 expression in injured MNs and positively correlated with MNs survival following BPRA injury. The transcription of ECEL1 is regulated by the transcription factors c-Jun and ATF3 in the context of BPRA injury, which is consistent with previous other nerve injuries study. In addition, the expression of TrkA gradually decreases in ECEL1-positive MNs and ECEL1 possibly preserves the activity of downstream AKT-GSK3β pathway of TrkA in injured MNs. In conclusion, our results introduce a promising therapeutic molecular target to assist re-implantation surgery for the treatment of BPRA injury.
ISSN:0893-7648
1559-1182
1559-1182
DOI:10.1007/s12035-023-03887-7