Expression and distribution of GAP‐43 in human astrocytes in culture

Moretto, Giuseppe; Ry, Xu; Monaco, Salvatore; Rizzuto, Nicolo’; Su, Kim

doi:10.1111/j.1365-2990.1995.tb01071.x

Cited by 7 publications

(6 citation statements)

References 22 publications

(7 reference statements)

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“…The characteristics of GAP-43 are somewhat like those of NOR-1, and GAP-43 probably has a role in glioma cell invasion [Maidment, 1997]. The cellular distribution of GAP-43 in this study was similar to that observed in cultured human astrocytes [Moretto et al, 1995]. The enhanced expression of GAP-43 caused by exposure to the magnetic field was transient and characterized by an early response (Fig.…”

Section: Discussionsupporting

confidence: 68%

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Exposure to power frequency magnetic fields and X‐Rays induces GAP‐43 gene expression in human glioma MO54 cells

Ding

Nakahara

Miyakoshi

2002

Bioelectromagnetics

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We investigated the distribution and expression of growth associated protein-43 (GAP-43) in human glioma cells (MO54) after exposure to a magnetic field (60 Hz, 5 mT), with or without initial X-ionizing radiation (2 Gy), by using immunocytochemistry and the reverse transcription polymerase chain reaction (RT-PCR). GAP-43 was present in the cytoplasm, accumulating in the perinuclear area. An increase in GAP-43 expression was observed with a peak at 10 h at the mRNA level and at 12 h at the protein level, after exposure to the magnetic field. The increased level of GAP-43 protein returned to a normal level within 24 h of exposure to a 5 mT magnetic field. The kinetic pattern of GAP-43 expression induced by X-ionizing radiation was very similar to that induced by the magnetic field. These results suggest that the stimulation of GAP-43 expression could occur by a similar mechanism following exposure to X-rays or magnetic fields. We have provided the first evidence that exposure to a 5 mT magnetic field can induce GAP-43 gene expression in human glioma MO54 cells.

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Section: Discussionsupporting

confidence: 68%

“…In addition, the distribution of GAP-43 is closely associated with cytoskeletal constituents, such as, e.g., glial fibrillary acidic protein (GFAP) [Moretto et al, 1995]. It is also known that GAP-43 can bind actin, although it does not directly affect actin polymerization and filament organization [Hens et al, 1993].…”

Section: Discussionmentioning

confidence: 99%

Exposure to power frequency magnetic fields and X‐Rays induces GAP‐43 gene expression in human glioma MO54 cells

Ding

Nakahara

Miyakoshi

2002

Bioelectromagnetics

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“…The non-neuronal cells included three neural-derived lines: naive PC12 cells, which are derived from chromaffin cells of the adrenal medulla; B1.1 Schwannoma cells; and C6 glioma cells. Cells from these neural lineages have been shown to express endogenous GAP-43 under some circumstances (Deloulme et al, 1993;Plantinga et al, 1993Plantinga et al, , 1994Costa et al, 1994;Moretto et al, 1995). However, under our culture conditions GAP-43 expression, if any, was below the level of detection for the chromaffin-and glial-derived lines.…”

Section: The Gap-43 Repressive Element Is Effective In a Wide Range Omentioning

confidence: 59%

Identification of a Novel Repressive Element That Contributes to Neuron-Specific Gene Expression

Weber

Skene

1997

J. Neurosci.

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Multiple signaling pathways are thought to control the selective expression of genes over the course of neuronal differentiation. One approach to elucidating these pathways is to identify specific cis-acting elements that serve as the final targets for these signaling pathways in neural-specific genes. We now identify a novel repressive element from the growth-associated protein 43 (GAP-43) gene that can contribute to neuron-specific gene expression by inhibiting transcription in a wide range of non-neuronal cell types. This repressive element is located downstream of the GAP-43 TATA box and is highly positiondependent. When transferred to viral promoters this element preferentially inhibits transcription in non-neuronal cells. Electrophoretic mobility shift assays show that the repressive element comprises at least two protein recognition sites. One of these is a novel sequence motif that we designate the SNOG element, because it occurs downstream of the TATA boxes of the synaptosomal-associated protein of 25 kDa and neuronal nitric oxide synthase genes, as well as the GAP-43 gene. The GAP-43 repressive element is distinct in sequence and position dependence from the repressor element 1/neuron-restrictive silencer element previously described in other neural genes and therefore is a likely target for a distinct set of signaling pathways involved in the control of neuronal differentiation.

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“…Previous investigations have demonstrated that astrocytes play a crucial role between the communications of neurons and BMECs 41-42. Therefore, neurons, BMECs, and astrocytes are the key components of NVU.…”

Section: Discussionmentioning

confidence: 98%

A Novel Brain Neurovascular Unit Model with Neurons, Astrocytes and Microvascular Endothelial Cells of Rat

Xue¹,

Liu²,

Hu³

et al. 2013

Int. J. Biol. Sci.

126

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A novel triple cell neurovascular unit (NVU) model co-culturing with neurons, brain microvascular endothelial cells (BMECs) and astrocytes was established in this study for investigating the cerebral diseases and screening the candidates of therapeutic drug. We have first performed the cell identification and morphological characterization, analyzed the specific protein expression and determined the blood-brain barrier (BBB) function of the co-culture model under normal condition. Then, we further determined the BBB function, inflammation, cell injury and the variation of neuroprotective factor in this model after anoxia-reoxygenation. The results suggest that this model exhibited a better BBB function and significantly increased expression of P-glycoprotein (Pg-P) and ZO-1 compared with BMECs only or co-culture with astrocytes or neurons. After anoxia-reoxygenation, the pathological changes of this model were basically resemblance to the pathological changes of brain cells and BBB in vivo. And nimodipine, an antagonist of calcium, could reverse those changes as well. According to our observations, we deduce that this triple cell co-culture model exhibits the basic structure, function and cell-cell interaction of NVU, which may offer a more proper in vitro system of NVU for the further investigation of cerebral diseases and drug screening.

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Expression and distribution of GAP‐43 in human astrocytes in culture

Cited by 7 publications

References 22 publications

Exposure to power frequency magnetic fields and X‐Rays induces GAP‐43 gene expression in human glioma MO54 cells

Exposure to power frequency magnetic fields and X‐Rays induces GAP‐43 gene expression in human glioma MO54 cells

Identification of a Novel Repressive Element That Contributes to Neuron-Specific Gene Expression

A Novel Brain Neurovascular Unit Model with Neurons, Astrocytes and Microvascular Endothelial Cells of Rat

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