PUBLICATION
Deletion of Slc1a4 Suppresses Single Mauthner Cell Axon Regeneration In Vivo through Growth-Associated Protein 43
- Authors
- Li, K., Fan, D., Zhou, J., Zhao, Z., Han, A., Song, Z., Tang, X., Hu, B.
- ID
- ZDB-PUB-241027-11
- Date
- 2024
- Source
- International Journal of Molecular Sciences 25(20): (Journal)
- Registered Authors
- Hu, Bing
- Keywords
- CNS axon regeneration, Gap43, single Mauthner cell, slc1a4, zebrafish
- MeSH Terms
-
- Excitatory Amino Acid Transporter 1/genetics
- Excitatory Amino Acid Transporter 1/metabolism
- Animals, Genetically Modified
- Gene Deletion
- GAP-43 Protein*/genetics
- GAP-43 Protein*/metabolism
- Tumor Suppressor Protein p53/genetics
- Tumor Suppressor Protein p53/metabolism
- Axons*/metabolism
- Axons*/physiology
- Disease Models, Animal
- Signal Transduction
- Spinal Cord Injuries*/genetics
- Spinal Cord Injuries*/metabolism
- Spinal Cord Injuries*/pathology
- Zebrafish*
- Nerve Regeneration*/genetics
- Zebrafish Proteins*/genetics
- Zebrafish Proteins*/metabolism
- Animals
- PubMed
- 39456733 Full text @ Int. J. Mol. Sci.
Citation
Li, K., Fan, D., Zhou, J., Zhao, Z., Han, A., Song, Z., Tang, X., Hu, B. (2024) Deletion of Slc1a4 Suppresses Single Mauthner Cell Axon Regeneration In Vivo through Growth-Associated Protein 43. International Journal of Molecular Sciences. 25(20):.
Abstract
Spinal cord injury (SCI) is a debilitating central nervous system (CNS) disorder that leads to significant motor and sensory impairments. Given the limited regenerative capacity of adult mammalian neurons, this study presents an innovative strategy to enhance axonal regeneration and functional recovery by identifying a novel factor that markedly promotes axonal regeneration. Employing a zebrafish model with targeted single axon injury in Mauthner cells (M-cells) and utilizing the Tg (Tol056: EGFP) transgenic line for in vivo monitoring, we investigate the intrinsic mechanisms underlying axonal regeneration. This research specifically examines the role of amino acid transport, emphasizing the role of the solute carrier 1A4 amino acid transporter in axonal regeneration. Our findings demonstrate that Slc1a4 overexpression significantly enhances axonal regeneration in M-cells, whereas Slc1a4 deficiency impedes this process, which is concomitant with the downregulation of the P53/Gap43 signaling pathway. By elucidating the fundamental role of Slc1a4 in axonal regeneration and uncovering its underlying mechanisms, this study thus provides novel insights into therapeutic strategies for SCI.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping