PUBLICATION
Glia maturation factor beta is required for reactive gliosis after traumatic brain injury in zebrafish
- Authors
- Yin, G., Du, M., Li, R., Li, K., Huang, X., Duan, D., Ai, X., Yao, F., Zhang, L., Hu, Z., Wu, B.
- ID
- ZDB-PUB-180418-43
- Date
- 2018
- Source
- Experimental neurology 305: 129-138 (Journal)
- Registered Authors
- Keywords
- Glia maturation factor beta, Microglia, Radial glial cells, Reactive gliosis, Traumatic brain injury
- MeSH Terms
-
- Animals
- Animals, Genetically Modified
- Brain Injuries, Traumatic/genetics
- Brain Injuries, Traumatic/metabolism*
- Brain Injuries, Traumatic/pathology
- Gene Knockdown Techniques/methods
- Glia Maturation Factor/biosynthesis*
- Glia Maturation Factor/genetics
- Glial Fibrillary Acidic Protein/biosynthesis
- Glial Fibrillary Acidic Protein/genetics
- Gliosis/genetics
- Gliosis/metabolism*
- Gliosis/pathology
- Male
- Mice
- Mice, Inbred BALB C
- Telencephalon/growth & development
- Telencephalon/metabolism
- Telencephalon/pathology
- Zebrafish
- PubMed
- 29655639 Full text @ Exp. Neurol.
Citation
Yin, G., Du, M., Li, R., Li, K., Huang, X., Duan, D., Ai, X., Yao, F., Zhang, L., Hu, Z., Wu, B. (2018) Glia maturation factor beta is required for reactive gliosis after traumatic brain injury in zebrafish. Experimental neurology. 305:129-138.
Abstract
Gliosis is a hallmark of neural pathology that occurs after most forms of central nervous system (CNS) injuries including traumatic brain injury (TBI). Identification of genes that control gliosis may provide novel treatment targets for patients with diverse CNS injuries. Glia maturation factor beta (GMFB) is crucial in brain development and stress response. In the present study, GMFB was found to be widely expressed in adult zebrafish telencephalon. A gmfb mutant zebrafish was created using CRISPR/cas9. In the uninjured zebrafish telencephalon, glial fibrillary acidic protein (GFAP) fibers in gmfb mutants were disorganized and shorter than wild type zebrafish. After TBI, transformation of quiescent type I radial glial cells (RGC) to proliferative type II RGCs was significantly suppressed in the gmfb mutant. RGC proliferation and hypertrophy post-TBI was reduced in gmfb mutants, indicating that reactive gliosis was attenuated. TBI-induced acute inflammation was also found to be alleviated in the gmfb mutant. Morphological changes also suggest attenuation of microglial reactive gliosis. In a mouse model of TBI, GMFB expression was increased around the injury site. These GMFB+ cells were identified as astrocytes and microglia. Taken together, the data suggests that GMFB is not only required for normal development of GFAP fibers in the zebrafish telencephalon, but also promotes reactive gliosis after TBI. Our findings provide novel information to help better understand the reactive gliosis process following TBI.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping