Glial Fibrillary Acidic Protein (GFA) in Normal Neural Cells and in Pathological Conditions

Bignami, A.; Dahl, D.; Rueger, David C.

doi:10.1016/b978-0-12-008301-5.50012-1

Cited by 194 publications

(87 citation statements)

References 94 publications

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“…Such agents have been used to inhibit glioma cell growth by changing their anaplastic phenotype in another more normal phenotype. Since differentiation status of glial cells can be assessed by glial fibrillary acidic protein (GFAP) [26], and the intensity of GFAP staining of glial tumors is inversely related to their degree of anaplasia [27], the effect of dobesilate in GFAP expression in those cells deserves future evaluation in longer exposure of culture treatment.…”

Section: Discussionmentioning

confidence: 99%

Dobesilate diminishes activation of the mitogen ‐ activated protein kinase ERK1/2 in glioma cells

Cuevas

Díaz-González

Garcia-Martin-Córdova

et al. 2006

J Cellular Molecular Medi

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Fibroblast growth factors (FGFs) and their receptors, regularly expressed at high levels in gliomas, are further upregulated during the transition of the tumor from low- to high-grade malignancy, and are essential for glioma progression. FGFs induce upregulation of the mitogen-activated protein kinase (MAPK) signaling cascade in cultured glioma cells, which suggests that MAPK pathway participates in the FGF-dependent glioma development. Recently, it has been shown that dobesilate, an inhibitor of FGF mitogenic activity, shows antiproliferative and proapoptotic activities in glioma cell cultures. Accordingly, it should be expected this new synthetic FGF inhibitor to affect the activation levels of MAPK. Here we report that immunocytochemical and Western blot data unequivocally show that treatment of cell cultures with dobesilate causes a significant decrease of the intracellular levels of ERK1/2 activation, one of the components of the MAPK signalling cascade. This finding supports an important role for dobesilate in glioma growth, suggesting that dobesilate should be a treatment to be born in mind for glioma management.

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Section: Discussionmentioning

confidence: 99%

Dobesilate diminishes activation of the mitogen ‐ activated protein kinase ERK1/2 in glioma cells

Cuevas

Díaz-González

Garcia-Martin-Córdova

et al. 2006

J Cellular Molecular Medi

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“…Considering that glial fibrillary acidic (GFA) protein has so far been thought to comprise a single protein species (review [2]), and also that astroglial filaments isolated from human gliosed brain were mainly composed of a single species of polypeptide of 49 000 M r [3], the simultaneous occurrence of two polypeptides in our purified astroglial filaments re'quires explanation.…”

Section: Introductionmentioning

confidence: 99%

“…), and washed with 150 mM NaC1, 0.1% NaN3 in 50 mM Tris-HC1 (pH 7.5). The gel was then treated with anti-GFA protein antiserum raised in a rabbit against the degraded antigen from the human spinal cord [2,11] followed by fluorescein isothiocyanate-conjugated IgG fraction of goat antiserum directed against rabbit IgG (Miles-Yeda, Israel) [12]. Photographs were taken under ultraviolet light.…”

Section: Direct Detection Of Gfa Protein By An Tibodymentioning

confidence: 99%

Astroglial filament and fibroblast intermediate filament proteins in cytoskeletal preparations from spinal cord and optic nerve

1981

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“…Recently, we detected laminin production by rat astrocytes in primary culture (Liesi et al, 1983a) and found that in cultured neuroblastoma cells the ultrastructural localization of laminin (Liesi, 1983) is compatible with a role for this glycoprotein in cell-to-cell and cellto-substratum interactions (Terranova et al, 1980;Ekblom et al, 1980;Liesi, 1983). Brain injury is known to exert a glial reaction that involves a conversion of the protoplasmic astrocytes of the gray matter into reactive astrocytes positive for glial fibrillary acidic protein (GFAP) (Bignami and Dahl, 1974b;Bignami et al, 1980). We now report that lesioning of the rat brain by stereotaxic injection of kainic acid, a selective neurotoxin destroying neostriatal nerve cell bodies (Coyle and Schwarcz, 1976;McGeer and McGeer, 1981;Garthwaite and Garthwaite, 1983), induces laminin in reactive astrocytes.…”

Section: Introductionmentioning

confidence: 99%

Laminin is induced in astrocytes of adult brain by injury.

Liesi¹,

Kaakkola²,

Dahl³

et al. 1984

The EMBO Journal

306

116

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Laminin is a high mol. wt. non-collagenous matrix glycoprotein, confined in adult tissues to basement membranes. In normal rat brain we found laminin mainly in vessel walls but, after injury, induced by stereotaxic injection of a neurotoxin, laminin immunoreactivity appeared also in reactive astrocytes, which are characteristically positive for the glial fibrillary acidic protein (GFAP). Laminin was first detected in GFAPimmunoreactive glial cells 24 h after injury. Four days later the majority of reactive astrocytes in the gray matter were positive for laminin and the laminin immunoreactivity, but not that of GFAP, gradually subsided within a month. Fibronectin, the other major matrix glycoprotein, was found only in capillary structures both in normal and lesioned brain tissue. The results indicate that mature astrocytes have the potential to produce laminin and suggest a role for this glycoprotein in brain regeneration.

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Glial Fibrillary Acidic Protein (GFA) in Normal Neural Cells and in Pathological Conditions

Cited by 194 publications

References 94 publications

Dobesilate diminishes activation of the mitogen ‐ activated protein kinase ERK1/2 in glioma cells

Dobesilate diminishes activation of the mitogen ‐ activated protein kinase ERK1/2 in glioma cells

Astroglial filament and fibroblast intermediate filament proteins in cytoskeletal preparations from spinal cord and optic nerve

Laminin is induced in astrocytes of adult brain by injury.

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