Tumor Necrosis Factor‐α and Basic Fibroblast Growth Factor Decrease Glial Fibrillary Acidic Protein and Its Encoding mRNA in Astrocyte Cultures and Glioblastoma Cells

Murphy, Greer M.; Lee, Yuen Ling; Jia, Xiao‐Chi; Yu, Annie; Majewska, Ania K.; Song, Yali; Schmidt, K. G.; Eng, Lawrence F.

doi:10.1046/j.1471-4159.1995.65062716.x

Cited by 31 publications

(13 citation statements)

References 13 publications

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“…In this context, it is interesting to note that decreased GFAP expression by astrocytes has previously been described in central pontine myelinolysis [8]. Furthermore, in vitro experiments have shown that GFAP is downregulated in astrocytes from mature brain in response to tumour necrosis factor‐α, and in fetal astrocytes, in response to IL‐1β[14,16,22]. Combined, these observations suggest that the reciprocal relationship in expression of peripherin and GFAP may be cytokine‐mediated.…”

Section: Discussionmentioning

confidence: 82%

Expression of peripherin in the brain of macaques (Macaca mulatta and Macaca fascicularis) occurs in astrocytes rather than neurones and is associated with encephalitis

Mathew

Westmoreland

Álvarez

et al. 2001

Neuropathology Appl Neurobio

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Peripherin is a member of the type III intermediate filament family, expressed in neurones of the peripheral nervous system of many species and in a discrete subpopulation of neurones of the central nervous system (CNS) during early development in rodents. Previous studies on rats have shown that peripherin immunoreactivity increased significantly in cell bodies of spinal motor neurones following axonal injury. Our study examined the expression of peripherin in the cerebrum of normal macaques (Macaca mulatta and Macaca fascicularis) and those with encephalitis of viral (simian immunodeficiency virus and simian virus 40) or autoimmune (experimental allergic encephalomyelitis) aetiology. Immunohistochemistry, immunoelectronmicroscopy, immunofluorescence and confocal microscopy were performed on tissue sections using antibodies against cell-specific markers and peripherin. Peripherin-positive cells were absent in the cerebrum of normal macaques of all ages examined, whereas animals with encephalitis had peripherin-positive cells associated with inflammatory infiltrates. Further evaluation revealed that these peripherin-positive cells were not neurones, but were predominantly astrocytes expressing glial fibrillary acidic protein. Our study suggests that peripherin is not neurone-specific in the CNS of macaques; peripherin is expressed in astrocytes of animals with encephalitis.

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Section: Discussionmentioning

confidence: 82%

Expression of peripherin in the brain of macaques (Macaca mulatta and Macaca fascicularis) occurs in astrocytes rather than neurones and is associated with encephalitis

Mathew

Westmoreland

Álvarez

et al. 2001

Neuropathology Appl Neurobio

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“…We chose U373 cells as these are a well-characterized model of cultured glial cells that retain many of the responses of primary astrocytes (Murphy et al, 1995;Blom et al, 1997). A23187 treatment of U373 cells strongly induced binding of nuclear proteins to two different NFAT consensus sites, from the IL-2 and VIP promoters (Fig.…”

Section: Resultsmentioning

confidence: 99%

NFAT4 is expressed in primary astrocytes and activated by glutamate

Jones

Sun

Kobierski

et al. 2003

J of Neuroscience Research

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Calcium signaling is a critical component of astrocyte activation but little information is available regarding the identity and function of transcriptional targets of calcium signaling in these cells. As a first step in elucidating the mechanisms that astrocytes use to regulate transcription in response to raised intracellular calcium concentrations, we have investigated expression and activation of the calcium activated transcription factors of the NFAT family. We report here that NFAT4 is expressed in U373 astrocytoma cells and in primary cultures of astrocytes. Treatment of U373 cells or primary astrocytes with the calcium ionophore A23187, or the neurotransmitter glutamate, leads to NFAT nuclear translocation and increased DNA binding to a NFAT consensus site through a cyclosporin A-sensitive process. These data suggest that NFAT4 functions as a calcium-responsive transcription factor in astrocytes.

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“…Concerning the astroglial cell number and cell trophy (GFAP expression), it’s reported that activated microglia enhance the astrocyte growth but do not have a hypertrophic effect on astrocyte (Rohl et al , 2007). Besids, proinflammatory cytokines like IL-1 and TNFα are reported to produce a decrease of GFAP expression in astrocyte culture (Selmaj et al , 1991; Oh et al , 1993; Lee et al , 1995; Murphy et al , 1995). It’s speculated that activated microglia might be to a great extent involved in the onset of astrogliosis but other or additional cell interaction might be responsible for the typical increase of GFAP in astrogliosis.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E2 released from activated microglia enhances astrocyte proliferation in vitro

Zhang

et al. 2009

Toxicology and Applied Pharmacology

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Microglial activation has been implicated in many astrogliosis-related pathological conditions including astroglioma; however, the detailed mechanism is not clear. In this study, we used primary enriched microglia and astrocytes cultures to determine the role of microglial prostaglandin E2 (PGE2) in the proliferation of astrocytes. The proliferation of astrocytes was measured by BrdU incorporation. The level of PGE2 was measured by ELISA method. Pharmacological inhibition or genetic ablation of COX-2 in microglia were also applied in this study. We found that proliferation of astrocytes increased following lipopolysaccharide (LPS) treatment in the presence of microglia. Furthermore, increased proliferation of astrocytes was observed in the presence of conditioned media from LPS-treated microglia. The potential involvement of microglial PGE2 in enhanced astrocyte proliferation was suggested by the findings that PGE2 production and COX-2 expression in microglia were increased by LPS treatment. In addition, activated microglia-induced increases in astrocyte proliferation were blocked by the PGE2 antagonist AH6809, COX-2 selective inhibitor DuP-697 or by genetic knockout of microglial COX-2. These findings were further supported by the finding that addition of PGE2 to the media significantly induced astrocyte proliferation. These results indicate that microglial PGE2 plays an important role in astrocyte proliferation, identifying PGE2 as a key neuroinflammatory molecule that triggers the pathological response related to uncontrollable astrocyte proliferation. These findings are important in elucidating the role of activated microglia and PGE2 in astrocyte proliferation and in suggesting a potential avenue in the use of anti-inflammatory agents for the therapy of astroglioma.

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Tumor Necrosis Factor‐α and Basic Fibroblast Growth Factor Decrease Glial Fibrillary Acidic Protein and Its Encoding mRNA in Astrocyte Cultures and Glioblastoma Cells

Cited by 31 publications

References 13 publications

Expression of peripherin in the brain of macaques (Macaca mulatta and Macaca fascicularis) occurs in astrocytes rather than neurones and is associated with encephalitis

Expression of peripherin in the brain of macaques (Macaca mulatta and Macaca fascicularis) occurs in astrocytes rather than neurones and is associated with encephalitis

NFAT4 is expressed in primary astrocytes and activated by glutamate

Prostaglandin E2 released from activated microglia enhances astrocyte proliferation in vitro

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