Neuronal modulation of schwann cell glial fibrillary acidic protein (GFAP)

Mokuno, Kenji; Kamholz, John; Behrman, T.; Black, Carolyn M.; Sessa, Maria; Feinstein, Douglas L.; Lee, V.; Pleasure, David E

doi:10.1002/jnr.490230405

Cited by 49 publications

(43 citation statements)

References 53 publications

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“…GFAP is an intermediate-filament protein expressed primarily in astrocytes and Schwann cells (18) and is well characterized histocytochemically (19,20). Modulation of GFAP gene expression during development, wound healing, and disease has been observed (21)(22)(23).…”

mentioning

confidence: 99%

Tissue-specific versus cell type-specific expression of the glial fibrillary acidic protein.

Kaneko

Sueoka

1993

Proc. Natl. Acad. Sci. U.S.A.

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Expression of the glial cell-specific gene encoding glial fibrillary acidic protein (GFAP) is regulated in a tissue-specific (neural tissue versus other tissues) as well as a cell type-specific (glial cell versus neuron) manner. Using a family of rat neurotumor RT4 cell lines in which neuronal/glial differentiation occurs in vitro, along with cell lines of different tissue origins, we identified by transient- and permanent-transfection assays two negative regulatory regions, GFAP downstream regulators 1 and 2 (GDR1 and GDR2). Both regions lie 3' of the transcription start site; GDR1 is in a 2.7-kb region extending from the first intron through the fifth exon, and GDR2 is within 1.7 kb 3' of the polyadenylylation site. GDR1 alone is responsible for tissue-specific expression (suppression in nonneural tissues), while both GDR1 and GDR2 are necessary for cell type-specific expression (suppression in neuronal cells).

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confidence: 99%

Tissue-specific versus cell type-specific expression of the glial fibrillary acidic protein.

Kaneko

Sueoka

1993

Proc. Natl. Acad. Sci. U.S.A.

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“…Axons and agents that elevate cAMP, such as forskolin (Fsk) (10), induce SCs freshly dissociated from nerve (primary SCs) to increase their expression of Po and myelin basic protein and dramatically decrease the expression ofNGFR (11). In primary SCs, the induction ofP0 by Fsk appears to occur only if the proliferative response of SCs to cAMP is prevented (12).…”

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confidence: 99%

Mitogen-expanded Schwann cells retain the capacity to myelinate regenerating axons after transplantation into rat sciatic nerve.

Feltri

Scherer

Wrabetz

et al. 1992

Proc. Natl. Acad. Sci. U.S.A.

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We have developed a method for genetically modifying Schwann cells (SCs) in vitro and then assed whether these SCs could interact normally with axons in vivo. Rat SCs were transduced in vitro with the IacZ gene by using a retroviral vector and then expanded with the SC mitogens forskolin and gllal growth factor. These mitogen-expanded SCs had an abnormal phenotype as compared to both SCs in vivo and primary SCs in vitro, yet when they were introduced into a regenerating rat sciatic nerve, they formed morphologically normal myelin sheaths around the axons. These results demonstrate that SCs can be genetically altered, their numbers expanded in culture, and yet respond appropriately to axonal signals in the peripheral nervous system. This approach offers a plausible way to manipulate genes involved in axon-SC interactions, including genes that may be defective in some inherited peripheral neuropathies.

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“…Acute infection in immunocompetent mice is generally restricted to approximately 3 to 7 dpi (25,41). Latent infection of sensory neurons persists after clearance of the acute infection (40,51). During this phase, infectious virus and viral antigen cannot be detected, and viral transcription is limited.…”

Section: Discussionmentioning

confidence: 99%

“…Seven-micrometer sections of latently infected trigeminal ganglia were deparaffinized with ClearRite III, xylene, and ethanol. Sections were labeled for glial fibrillary acidic protein (GFAP), a marker for Schwann cells (5,12,16,40,47,62), or neurofilament protein, a marker for neurons (15), by the avidin-biotin-peroxidase method (Vector). Diaminobenzidine tetrahydrochloride (DAB) was used as the substrate.…”

Section: Methodsmentioning

confidence: 99%

The Transgenic ICP4 Promoter Is Activated in Schwann Cells in Trigeminal Ganglia of Mice Latently Infected with Herpes Simplex Virus Type 1

Taus

Mitchell

2001

J Virol

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Herpes simplex virus type 1 (HSV-1) establishes a latent infection in peripheral sensory ganglionic neurons in humans and in the mouse model. Latent infection in ganglionic neurons is the means by which HSV-1 remains in infected humans for years. Periodic reactivation of latent infection results in spread of the virus to naive hosts. The mechanism of regulation of the latent viral genome in neurons has been intensively investigated in mouse models. Many studies utilizing in situ hybridization in mice and in humans have shown that transcription from the latent HSV-1 genome in neurons is limited to RNA that maps to the gene coding for latency-associated transcripts (LATs) (reviewed in references 17, 50, and 59). In contrast, lytic viral infection is characterized by an ordered cascade of viral gene expression: immediate-early (IE) genes are expressed first followed by early and late genes (43). Based on these findings, it has been hypothesized that latent infection of sensory neurons requires the absence of viral IE gene expression (reviewed in references 18 and 20). According to this hypothesis, reactivation of HSV-1 from latency is dependent upon activation or loss of repression of viral IE gene expression in neurons (20,41,43). IE genes would then activate the lytic cycle of viral gene expression, leading to the production of infectious virus. Some studies utilizing reverse transcription-PCR (RT-PCR) have demonstrated the presence of viral IE (ICP4) transcripts in homogenates of trigeminal ganglia from mice latently infected with 26). These studies have raised the question of whether HSV-1 IE genes are transcribed in neurons during latent infection.Trigeminal ganglia are comprised of multiple cell types, including Schwann cells, satellite cells, and different types of neurons (31,45,53). In order to understand the significance of the finding of ICP4 mRNA in latently infected sensory ganglia, it is important to know whether the ICP4 transcription originates from neurons. Presently available techniques such as in situ hybridization are not sensitive enough to localize the ICP4 transcripts to specific cells. It is possible to examine by very sensitive methods which specific cells activate the HSV-1 ICP4 promoter in latently infected trigeminal ganglia. Activation of the ICP4 promoter in neurons would be required for production of ICP4 transcripts in latently infected neurons.We used reporter transgenic mice containing the HSV-1(F) ICP4 promoter fused to the ␤-galactosidase coding sequence to assay for HSV-1 ICP4 promoter activation in specific cells in latently infected trigeminal ganglia. Promoter transgenic mice were inoculated by the intracorneal route with HSV-1(F) to determine whether neurons in trigeminal ganglia activated the ICP4 promoter during latency. Trigeminal ganglia were assayed for ␤-galactosidase-positive cells at 5, 11, 23, and 37 days postinoculation (dpi). Moderate numbers of neurons and nonneuronal cells in trigeminal ganglia were positive for ␤-galactosidase at 5 dpi. The number of positive n...

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Neuronal modulation of schwann cell glial fibrillary acidic protein (GFAP)

Cited by 49 publications

References 53 publications

Tissue-specific versus cell type-specific expression of the glial fibrillary acidic protein.

Tissue-specific versus cell type-specific expression of the glial fibrillary acidic protein.

Mitogen-expanded Schwann cells retain the capacity to myelinate regenerating axons after transplantation into rat sciatic nerve.

The Transgenic ICP4 Promoter Is Activated in Schwann Cells in Trigeminal Ganglia of Mice Latently Infected with Herpes Simplex Virus Type 1

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