Your browser doesn't support javascript.
loading
Brachial Plexus Root Avulsion Injury-Induced Endothelin-Converting Enzyme-Like 1 Overexpression Is Associated with Injured Motor Neurons Survival.
Huang, Yu; Mai, Yunlin; Ye, Weijian; Lv, Shiqin; Zhou, Yingying; Wu, Pingzhen; Zhou, Lihua; Li, Yingqin; Zhong, Ke.
Afiliación
  • Huang Y; Department of Anatomy, School of Medicine (Shenzhen), Sun Yat-sen University, Shenzhen, Guangdong, China.
  • Mai Y; Department of Anatomy, School of Medicine (Shenzhen), Sun Yat-sen University, Shenzhen, Guangdong, China.
  • Ye W; Center of Cyclotron and PET Radiopharmaceuticals, Department of Nuclear Medicine and PET/CT-MRI Center, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China.
  • Lv S; Department of Anatomy, School of Medicine (Shenzhen), Sun Yat-sen University, Shenzhen, Guangdong, China.
  • Zhou Y; Department of Anatomy, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China.
  • Wu P; Department of Anatomy, School of Medicine (Shenzhen), Sun Yat-sen University, Shenzhen, Guangdong, China.
  • Zhou L; Department of Anatomy, School of Medicine (Shenzhen), Sun Yat-sen University, Shenzhen, Guangdong, China.
  • Li Y; Department of Radiology, The Fifth Affiliated Hospital, Sun Yat-sen University, 52 Mei Hua East Road, Zhuhai, 519000, Guangdong, China. liyqin@mail.sysu.edu.cn.
  • Zhong K; Department of Pharmacy, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, 107 Yanjiang West Road, Guangzhou, 510120, Guangdong, China. zhongk9@mail.sysu.edu.cn.
Mol Neurobiol ; 61(8): 5194-5205, 2024 Aug.
Article en En | MEDLINE | ID: mdl-38170441
ABSTRACT
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-GSK3ß 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.
Asunto(s)
Palabras clave

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Plexo Braquial / Supervivencia Celular / Neuronas Motoras Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Animals Idioma: En Revista: Mol Neurobiol Asunto de la revista: BIOLOGIA MOLECULAR / NEUROLOGIA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Plexo Braquial / Supervivencia Celular / Neuronas Motoras Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Animals Idioma: En Revista: Mol Neurobiol Asunto de la revista: BIOLOGIA MOLECULAR / NEUROLOGIA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos