Increase in glial fibrillary acidic protein following neural trauma

Vijayan, Vijaya K.; Lee, Y. L.; Eng, Lawrence F.

doi:10.1007/bf03159912

Cited by 72 publications

(38 citation statements)

References 34 publications

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“…The second aim was to compare changes in diffusion parameters to the degree of astrogliosis and CSPG expression. The time course of astrogliosis in our study was in agreement with previous findings (Bignami and Dahl, 1974;Mathewson and Berry, 1985;Lindsay, 1986;Hozumi et al, 1990;Vijayan et al, 1990;Hatten et al, 1991;Norton et al, 1992;Bignami and Dahl, 1995), showing that the level of GFAP in the wounded hemisphere was increased as early as 3 days post-lesion; it was most prominent at 7 days ( Fig. 1) and declined at 21 and 35 days.…”

Section: Results Immunocytochemistrysupporting

confidence: 94%

Diffusion barriers evoked in the rat cortex by reactive astrogliosis

Roitbak

Syková

1999

Glia

189

142

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Changes in extracellular space (ECS) diffusion parameters in astrogliotic tissue around a unilateral cortical stab wound were determined from concentrationtime profiles of tetramethylammonium (TMA ϩ ) using TMA ϩ -selective microelectrodes. Three diffusion parameters-ECS volume fraction ␣ (␣ ϭ ECS volume/ total tissue volume), tortuosity ( 2 ϭ D/ADC; where D is the free and ADC is the apparent diffusion coefficient of TMA ϩ in the brain), and nonspecific TMA ϩ uptake kЈ-were determined at 3, 7, 21, and 35 days postwounding (dpw), in the hemispheres ipsilateral and contralateral to the lesion. Following diffusion experiments, tissue sections were immunostained for glial fibrillary acidic protein (GFAP) and chondroitin-sulphate proteoglycans (CSPG). In the area 300-1000 µm around the wound, ␣ was increased at 3, 7, and 21 dpw by about 20% but returned to control values at 35 dpw; was increased at all four intervals, reaching a maximum at 7 dpw. kЈ was lower than in the contralateral hemisphere at 7, 21, and 35 dpw. Measurements 1,500-2,000 µm from the wound revealed only an increase in at 7 dpw. The time course of changes in ECS diffusion parameters closely correlated with increased staining for GFAP and CSPG. Our results show that astrogliosis significantly changes the diffusion properties of nervous tissue, making it less permissive. Both hypertrophied astrocytic processes and an enhanced formation of some extracellular matrix molecules could affect, through changes in the diffusion of molecules in the ECS, neuron-glia communication, ''cross-talk'' between synapses, extrasynaptic transmission, and regenerative processes.

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Section: Results Immunocytochemistrysupporting

confidence: 94%

Diffusion barriers evoked in the rat cortex by reactive astrogliosis

Roitbak

Syková

1999

Glia

189

142

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“…We speculated that the higher levels of XT-I and -II mRNA in 3 week-old primary astrocyte cultures reflected that these cultures were in an activated state induced by the isolation procedure. This speculation was supported by the observation that the expression of GFAP, a gene expressed by reactive astrocytes following CNS injury (Janeczko, 1988;Vijayan et al, 1990) was also elevated in 3-week-old compared with 6-week-old astrocyte cultures (Fig. 4B).…”

Section: Characterization Of Cbg Expression In Primary Astrocyte Cultmentioning

confidence: 79%

Transcriptional regulation of scar gene expression in primary astrocytes

Gris

Tighe

Levin

et al. 2007

Glia

115

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The failure of the adult injured spinal cord to support axonal regeneration is in part attributed to the glial scar. Reactive astrocytes constitute a major cellular component of the glial scar and are heterogeneous with respect to the extracellular matrix proteins that they secrete. Astrocytes may produce antiregenerative molecules such as chondroitin sulphate proteoglycans (CSPGs) or proregenerative molecules such as laminin and fibronectin. While many different CSPGs are expressed after spinal cord injury (SCI) they all rely on the same enzymes, xylosyltransferase-I and -II (XT-I, XT-II) and chondroitin 4-sulfotransferase (C4ST) to add the repulsive chondroitin sulfate side chains to their core proteins. We show that XT-I, XT-II, and C4ST are part of a CSPG biosynthetic gene (CBG) battery. Using primary astrocyte cultures and quantitative PCR we demonstrate that TGFbeta2, PDGF, and IL-6 induce the expression of CBGs, laminin and fibronectin by several-fold. We further show that over-expression of the transcription factor SOX9 also strongly induces the expression of CBGs but does not increase the expression of laminin or fibronectin. Correspondingly, SOX9 knock-down in primary astrocytes causes a decrease in CBG and an increase in laminin and fibronectin mRNA levels. Finally, we show that the in vivo expression profiles of TGFbeta2, PDGF, IL-6, and SOX9 are consistent with their potential roles in differentially regulating CBGs, laminin and fibronectin gene expression in the injured spinal cord. This work suggests that SOX9 levels may be pivotal in determining the balance of pro- and anti-regenerative extracellular matrix molecules produced by astrocytes.

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“…Astrocytes appeared hypertrophic with thick processes stained heavily for their intermediate filament protein GFAP (glial fibrillary acidic protein) as described previously (Vijayan et al, 1990). Double staining with anti-GFAP and anti-vimentin antibodies showed that astrocytes near the lesion site were vimentin positive (data not shown).…”

Section: General Observationsmentioning

confidence: 94%

Chemokine expression in rat stab wound brain injury

Ghirnikar

Lee

et al. 1996

J. Neurosci. Res.

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A traumatic injury to the adult mammalian central nervous system (CNS) results in reactive astrogliosis and the migration of hematogenous cells into the damaged neural tissue. Chemokines, a novel class of chemoattractant cytokines, are now being recognized as mediators of the inflammatory changes that occur following injury. The expression of MCP‐1 (macrophage chemotactic peptide‐1), a member of the β family of chemokines, has recently been demonstrated in trauma in the rat brain (Berman et al.: J Immunol 156:3017–3023, 1996). Using a stab wound model for mechanical injury, we studied the expression of two other β chemokines: RANTES (Regulated on Activation, Normal T cell Expressed and Secreted) and MIP‐1 β (macrophage inflammatory protein‐1 beta) in the rat brain. The stab wound injury was characterized by widespread gliosis and infiltration of hematogenous cells. Immunohistochemical staining revealed the presence of RANTES and MIP‐1 β in the injured brain. RANTES and MIP‐1 β were both diffusely expressed in the necrotic tissue and were detected as early as 1 day post‐injury (dpi). Double‐labeling studies showed that MIP‐1 β, but not RANTES, was expressed by reactive astrocytes near the lesion site. In addition, MIP‐1 β staining was also detected on macrophages at the site of injury. The initial expression of the chemokines closely correlated with the appearance of inflammatory cells in the injured CNS, suggesting that RANTES and MIP‐1 β may play a role in the inflammatory events of traumatic brain injury. This study also demonstrates for the first time MIP‐1 β expression in reactive astrocytes following trauma to the rat CNS. © 1996 Wiley‐Liss, Inc.

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Increase in glial fibrillary acidic protein following neural trauma

Cited by 72 publications

References 34 publications

Diffusion barriers evoked in the rat cortex by reactive astrogliosis

Diffusion barriers evoked in the rat cortex by reactive astrogliosis

Transcriptional regulation of scar gene expression in primary astrocytes

Chemokine expression in rat stab wound brain injury

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