title: FABP7 expression in normal and stab-injured brain cortex and its role in astrocyte proliferation.
abstract: Reactive gliosis, in which astrocytes as well as other types of glial cells undergo massive proliferation, is a common hallmark of all brain pathologies. Brain-type fatty acid-binding protein (FABP7) is abundantly expressed in neural stem cells and astrocytes of developing brain, suggesting its role in differentiation and/or proliferation of glial cells through regulation of lipid metabolism and/or signaling. However, the role of FABP7 in proliferation of glial cells during reactive gliosis is unknown. In this study, we examined the expression of FABP7 in mouse cortical stab injury model and also the phenotype of FABP7-KO mice in glial cell proliferation. Western blotting showed that FABP7 expression was increased significantly in the injured cortex compared with the contralateral side. By immunohistochemistry, FABP7 was localized to GFAP(+) astrocytes (21% of FABP7(+) cells) and NG2(+) oligodendrocyte progenitor cells (62%) in the normal cortex. In the injured cortex there was no change in the population of FABP7(+)/NG2(+) cells, while there was a significant increase in FABP7(+)/GFAP(+) cells. In the stab-injured cortex of FABP7-KO mice there was decrease in the total number of reactive astrocytes and in the number of BrdU(+) astrocytes compared with wild-type mice. Primary cultured astrocytes from FABP7-KO mice also showed a significant decrease in proliferation and omega-3 fatty acid incorporation compared with wild-type astrocytes. Overall, these data suggest that FABP7 is involved in the proliferation of astrocytes by controlling cellular fatty acid homeostasis.
authors.affiliation: Department of Organ Anatomy, Yamaguchi University Graduate School of Medicine, Ube, Japan.
authors.forename: Kazem
authors.initials: K
authors.lastname: Sharifi
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Morihiro
authors.forename: Motoko
authors.initials: M
authors.lastname: Maekawa
authors.forename: Yuki
authors.initials: Y
authors.lastname: Yasumoto
authors.forename: Hisae
authors.initials: H
authors.lastname: Hoshi
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Adachi
authors.forename: Tomoo
authors.initials: T
authors.lastname: Sawada
authors.forename: Nobuko
authors.initials: N
authors.lastname: Tokuda
authors.forename: Hisatake
authors.initials: H
authors.lastname: Kondo
authors.forename: Takeo
authors.initials: T
authors.lastname: Yoshikawa
authors.forename: Michiyasu
authors.initials: M
authors.lastname: Suzuki
authors.forename: Yuji
authors.initials: Y
authors.lastname: Owada
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D000941:Antigens / Q000378:metabolism; D001253:Astrocytes / Q000378:metabolism* / Q000473:pathology; D049109:Cell Proliferation; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000293:injuries* / Q000378:metabolism*; D004195:Disease Models, Animal; D000071438:Fatty Acid-Binding Protein 7; D050556:Fatty Acid-Binding Proteins / Q000235:genetics / Q000378:metabolism*; D015525:Fatty Acids, Omega-3 / Q000378:metabolism; D015870:Gene Expression; D005911:Gliosis / Q000378:metabolism / Q000473:pathology; D006706:Homeostasis; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism*; D058953:Neural Stem Cells / Q000378:metabolism / Q000473:pathology; D009836:Oligodendroglia / Q000378:metabolism / Q000473:pathology; D011509:Proteoglycans / Q000378:metabolism; D014951:Wounds, Stab / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D000099216:Chondroitin Sulfate Proteoglycan 4
chemical_list: D000941:Antigens; D000071438:Fatty Acid-Binding Protein 7; D050556:Fatty Acid-Binding Proteins; D015525:Fatty Acids, Omega-3; D009419:Nerve Tissue Proteins; D011509:Proteoglycans; D000099216:Chondroitin Sulfate Proteoglycan 4; C086936:Fabp7 protein, mouse