title: Regional difference of reactive astrogliosis following traumatic brain injury revealed by hGFAP-GFP transgenic mice.
abstract: Reactive astrocytes greatly influence the wound healing and neuronal regeneration processes following brain injury. However, the origin and fate of reactive astrocytes appear to be different depending on the type, severity and duration of brain injury. Using the cryogenic traumatic brain injury model, here we comprehensively addressed the regional differences of reactive astrocytes in the injured cortex. In the proximal region of injury site, NG2-expressing and cytoplasmic Olig2-labeled cells were densely localized 3 days after the injury. Next to this proximal layer, most of reactive astrocytes did not express NG2 but exhibited radial glia-like shape with elongated processes. Accordingly, they expressed the progenitor or radial glial markers, such as vimentin, brain lipid binding protein (BLBP) and the green fluorescent protein (GFP) under the control of the human GFAP (hGFAP) promoter. However, only few glial fibrillary acidic protein (GFAP) expressing astrocytes were found in this layer. Distal to the injury site, most of astrocytes strongly expressed GFAP with hypertonic morphology. At day 15 after injury, all layers expressing GFAP and other marker expressions disappeared, indicating the termination of reactive astrogliosis. Taken together, our data suggest that reactive astrogliosis occurs in a regionally segregated manner in the early phase of brain injury.
authors.affiliation: Department of Anatomy, BK21 Program, Korea University College of Medicine, 126-1 Anam-Dong, Sungbuk-Gu, Seoul 136-705, Republic of Korea.
authors.forename: Woon Ryoung
authors.initials: WR
authors.lastname: Kim
authors.forename: Joo Yeon
authors.initials: JY
authors.lastname: Kim
authors.forename: Younghye
authors.initials: Y
authors.lastname: Moon
authors.forename: Hyun Jung
authors.initials: HJ
authors.lastname: Kim
authors.forename: Hyun
authors.initials: H
authors.lastname: Kim
authors.forename: Woong
authors.initials: W
authors.lastname: Sun
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000378:metabolism / Q000473:pathology*; D051792:Basic Helix-Loop-Helix Proteins / Q000378:metabolism; D001930:Brain Injuries / Q000378:metabolism / Q000473:pathology*; D002540:Cerebral Cortex / Q000293:injuries / Q000378:metabolism / Q000473:pathology*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000378:metabolism / Q000473:pathology*; D051379:Mice; D008822:Mice, Transgenic; D009419:Nerve Tissue Proteins / Q000378:metabolism; D000076104:Oligodendrocyte Transcription Factor 2
chemical_list: D051792:Basic Helix-Loop-Helix Proteins; D005904:Glial Fibrillary Acidic Protein; D009419:Nerve Tissue Proteins; D000076104:Oligodendrocyte Transcription Factor 2; C512773:Olig2 protein, mouse