1. Academic Validation
  2. Glia maturation factor beta is required for reactive gliosis after traumatic brain injury in zebrafish

Glia maturation factor beta is required for reactive gliosis after traumatic brain injury in zebrafish

  • Exp Neurol. 2018 Jul;305:129-138. doi: 10.1016/j.expneurol.2018.04.008.
Guo Yin 1 Mingjun Du 1 Rong Li 2 Ke Li 1 Xiaomin Huang 1 Dongbei Duan 1 Xiaolan Ai 1 Fang Yao 1 Lanlan Zhang 1 Ziyou Hu 1 Bingyi Wu 3
Affiliations

Affiliations

  • 1 Research Center of Clinical Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
  • 2 Department of Radiation Oncology, Affiliated Cancer Hospital, Institute of Guangzhou Medical University, No.78, Hengzhigang Road, Yuexiu District, Guangzhou 510095, Guangdong, China.
  • 3 Research Center of Clinical Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China. Electronic address: wubingyi66@126.com.
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.

Keywords

Glia maturation factor beta; Microglia; Radial glial cells; Reactive gliosis; Traumatic brain injury.

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