Possible association of platelet-derived growth factor (PDGF) with the appearance of reactive astrocytes following brain injury in situ

Takamiya, Yoshiaki; Kohsaka, Shinichi; Toya, Shigeo; Otani, Mitsuhiro; Mikoshiba, Katsuhiko; Tsukada, Yasuzo

doi:10.1016/0006-8993(86)90029-6

Cited by 56 publications

(15 citation statements)

References 12 publications

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“…Their specificities have been confirmed in previous papers for anti-GFAP (18,33) anti-S-100 (22). Anti-glutamine synthetase was raised in our laboratory by immunizing rabbits with purified sheep gluamine synthetase (Sigma, cat no.…”

Section: Immunohistochemistrysupporting

confidence: 59%

Differential response of three astrocyte-specific proteins to fimbrial transection of the rat brain: Immunohistochemical observations with antibodies against glial fibrillary acidic protein, glutamine synthetase and S-100 protein.

Tanaka¹,

Araki

Masuzawa

1991

Acta Histochem. Cytochem

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Section: Immunohistochemistrysupporting

confidence: 59%

Differential response of three astrocyte-specific proteins to fimbrial transection of the rat brain: Immunohistochemical observations with antibodies against glial fibrillary acidic protein, glutamine synthetase and S-100 protein.

Tanaka¹,

Araki

Masuzawa

1991

Acta Histochem. Cytochem

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“…28 Our findings are in agreement with those of previous studies, which have suggested a high level of expression of PDGF, hence a role in arteriogenesis, in reactive astrocytes and macrophages during brain injury. 29,30 Accordingly, the present findings may imply a process in which macrophages and reactive astrocytes in the gliotic zone express high levels of VEGF and PDGF, thus inducing gliosis. This, in turn, might increase the angiogenic activity within (in AVM) or around (in AVM and CCM) the lesions, since endothelial cells from these malformations are more prone to angiogenic stimuli through the PDGF pathway because they express higher levels of PDGF receptors.…”

Section: Loss Of Pdgf Receptor/ligand Mismatchmentioning

confidence: 60%

Expression of platelet-derived growth factor ligand and receptor in cerebral arteriovenous and cavernous malformations

Yıldırım

Biçer

Ozkan

et al. 2010

Journal of Clinical Neuroscience

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“…[67,72,112,113] Evidence exists that the local activation of astrocytes in these models is mediated by cytokines and growth factors including interleukin (IL)-1, IL-6, transforming growth factor-alpha, transforming growth factor-beta1, tumor necrosis factor-alpha, gamma-interferon, and basic fibroblast growth factor. [2,31,32,33,40,53,58,82,119,120] Interestingly, astrocytes have the highest predisposition to malignant transformation of any CNS cell type.…”

Section: Biological Features Of Astrocytesmentioning

confidence: 99%

Role of glial filaments in cells and tumors of glial origin: a review

Rutka¹,

Murakami²,

Dirks³

et al. 1997

FOC

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In the adult human brain, normal astrocytes constitute nearly 40% of the total central nervous system (CNS) cell population and may assume a star-shaped configuration resembling epithelial cells insofar as the astrocytes remain intimately associated, through their cytoplasmic extensions, with the basement membrane of the capillary endothelial cells and the basal lamina of the glial limitans externa. Although their exact function remains unknown, in the past, astrocytes were thought to subserve an important supportive role for neurons, providing a favorable ionic environment, modulating extracellular levels of neurotransmitters, and serving as spacers that organize neurons. In immunohistochemical preparations, normal, reactive, and neoplastic astrocytes may be positively identified and distinguished from other CNS cell types by the expression of the astrocyte-specific intermediate filament glial fibrillary acidic protein (GFAP). This GFAP is a 50-kD intracytoplasmic filamentous protein that constitutes a portion of, and is specific for, the cytoskeleton of the astrocyte. This protein has proved to be the most specific marker for cells of astrocytic origin under normal and pathological conditions. Interestingly, with increasing astrocytic malignancy, there is progressive loss of GFAP production. As the human gene for GFAP has now been cloned and sequenced, this review begins with a summary of the molecular biology of GFAP including the proven utility of the GFAP promoter in targeting genes of interest to the CNS in transgenic animals. Based on the data provided the authors argue cogently for an expanded role of GFAP in complex cellular events such as cytoskeletal reorganization, maintenance of myelination, cell adhesion, and signaling pathways. As such, GFAP may not represent a mere mechanical integrator of cellular space, as has been previously thought. Rather, GFAP may provide docking sites for important kinases that recognize key cellular substrates that enable GFAP to form a dynamic continuum with microfilaments, integrin receptors, and the extracellular matrix.

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Possible association of platelet-derived growth factor (PDGF) with the appearance of reactive astrocytes following brain injury in situ

Cited by 56 publications

References 12 publications

Differential response of three astrocyte-specific proteins to fimbrial transection of the rat brain: Immunohistochemical observations with antibodies against glial fibrillary acidic protein, glutamine synthetase and S-100 protein.

Differential response of three astrocyte-specific proteins to fimbrial transection of the rat brain: Immunohistochemical observations with antibodies against glial fibrillary acidic protein, glutamine synthetase and S-100 protein.

Expression of platelet-derived growth factor ligand and receptor in cerebral arteriovenous and cavernous malformations

Role of glial filaments in cells and tumors of glial origin: a review

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