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Fatty Acid Binding Protein 7 Is Involved in the Proliferation of Reactive Astrocytes, But Not in Cell Migration and Polarity Publisher



Hara T1, 2 ; Umaru BA1 ; Sharifi K3 ; Yoshikawa T2 ; Owada Y1 ; Kagawa Y1
Authors
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Authors Affiliations
  1. 1. Department of Organ Anatomy, Tohoku University Graduate School of Medicine, Sendai, 980–8575, Japan
  2. 2. Laboratory for Molecular Psychiatry, RIKEN Center for Brain Science, Wako, 351–0198, Japan
  3. 3. Department of Medical Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran

Source: Acta Histochemica et Cytochemica Published:2020


Abstract

Reactive gliosis is a defense mechanism to minimize and repair the initial damage after CNS injuries that is characterized by increases in astrocytic reactivity and proliferation, with enhanced expression of glial fibrillary acidic protein (GFAP) and cellular hypertrophy. Fatty acid binding protein 7 (FABP7) is abundantly expressed in several types of glial cells, such as astrocytes and oligodendrocyte precursor cells, during brain development and FABP7-positive astrocytes have been shown to be significantly increased in the mouse cortex after a stab injury. However, the functional significance of FABP7 in gliosis remains unclear. In the present study, we examined the mechanism of FABP7-mediated regulation of gliosis using an in vitro scratch-injury model using primary cultured astrocytes. Western blotting showed that FABP7 expression was increased significantly in scratch wounded astrocytes at the edge of the injury compared with intact astrocytes. Through monitoring the occupancy of the injured area, FAB7-KO astrocytes showed a slower proliferation rate compared with WT astrocytes after 48 hr, which was confirmed by BrdU immunostaining. There were no differences in cell migration and polarity of reactive astrocytes between FABP-KO and WT. Conclusively, our data suggest that FABP7 is important in the proliferation of reactive astrocytes in the context of CNS injury. © 2020 The Japan Society of Histochemistry and Cytochemistry.