Differential regulation of myelin gene expression in SV40 T antigen-transfected rat glioma C6 cells

Bong, M.; Chakrabarti, Arun K.; Banik, Naren L.; Hogan, Edward L.; Kanoh, Makoto; Wiggins, R. C.; Konat, G.

doi:10.1007/bf01000381

Cited by 16 publications

(11 citation statements)

References 36 publications

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“…Early passage C6 cells used in this study express low amounts of the MAG mRNA (Bong et al, 1991;Kanoh et al, 1991), but when normalized to the total RNA it is only approximately one three hundredth of that in oligodendrocytes (Konat, unpublished observation). The MAG gene expression in C6 cells can be upregulated approximately 50-fold by treatment with CAMP potentiator, i.e., isoproterenol (Ye et al, 1992(Ye et al, , 1994.…”

Section: Resultsmentioning

confidence: 98%

“…In the actively myelinating brain employed in this study (25-30 day postpartum), the gene activity normalized to the total RNA was about four fold lower than in purified oligodendrocytes, which approximately reflects the proportion of oligodendrocytes within cellular population of the tissue. Early passage C6 cells used in this study express low amounts of the MAG mRNA (Bong et al, 1991;Kanoh et al, 1991), but when normalized to the total RNA it is only approximately one three hundredth of that in oligodendrocytes (Konat, unpublished observation). The MAG gene expression in C6 cells can be upregulated approximately 50-fold by treatment with CAMP potentiator, i.e., isoproterenol (Ye et al, 1992(Ye et al, , 1994.…”

Section: Resultsmentioning

confidence: 99%

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Differentiation‐specific demethylation of myelin associated glycoprotein gene in cultured oligodendrocytes

Grubinska

Laszkiewicz

Royland

et al. 1994

J of Neuroscience Research

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The methylation status of a 4.4-kb 5' end of the myelin-associated glycoprotein (MAG) gene was assessed in cells with different levels of transcriptional activity of the gene, i.e., liver, brain, O-2A oligodendrocyte precursors cells, mature oligodendrocytes, and glioma C6 cells. Purified DNA was digested with methylation-sensitive restriction enzymes, and the cuts were mapped by the indirect end-labeling technique. The restriction sites within the 4.4-kb fragment revealed a highly heterogenous methylation pattern among cells and tissues, and liver DNA was the most heavily methylated. Most of the restriction sites were partly demethylated in the nervous system cells. Notably, two adjacent Hha1 sites at +94 and +96 were fully methylated in liver, but partially demethylated in the brain, OL, and O2A. Two Hpa2 site located at -1836 and at -39 were progressively demethylated in oligodendrocyte lineage cells, indicating specific hypomethylation associated with the oligodendrocytic differentiation. Most of the restriction sites were weakly methylated in the DNA from neoplastic C6 cells, although the Hha1 sites were fully methylated. No clear-cut correlation between the extent of CpG dinucleotide methylation and the chromatin conformation was found. For example, out of four heavily methylated sites only two comapped with MNase hypersensitive sites. Also, the -1836 Hpa2 site whose demethylation is concomitant with oligodendrocytic differentiation seems to be localized within precisely positioned nucleosomal arrays of the MAG gene chromatin. The results indicate that the MAG gene undergoes progressive demethylation concomitant with the oligodendrocyte differentiation/maturation. However, certain CpG dinucleotides remain heavily methylated even in the fully active gene in mature oligodendrocytes, indicating that they may be essential in maintaining proper chromatin structure.

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Section: Resultsmentioning

confidence: 98%

Section: Resultsmentioning

confidence: 99%

Differentiation‐specific demethylation of myelin associated glycoprotein gene in cultured oligodendrocytes

Grubinska

Laszkiewicz

Royland

et al. 1994

J of Neuroscience Research

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“…The aim of this study was to evaluate possible involvement of cAMP in the regulation of PLP and myelinassociated glycoprotein (MAG) gene expression in rat glioma C6 cells. These cells express several myelin-specific genes, namely, CNP, PLP and MAG, and the expression can be experimentally modified (McMoms, 1983;McMorris et al, 1985;Bong et al, 1991;Konat et al, 1991b;Nave and Lemke, 1991). Since isoproterenol, a P-adrenergic receptor agonist, transiently increases cAMP level in C6 cells (Gilman and Nirenberg,197 1 ; Sharma and Raj , 1987), we employed it as a model drug along with propranolol, a P-antagonist, and forskolin, an adenylate cyclase activator.…”

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confidence: 99%

Cyclic AMP‐induced upregulation of proteolipid protein and myelin associated glycoprotein gene expression in C6 cells

Ye¹,

Kanoh²,

Zhu³

et al. 1992

J of Neuroscience Research

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A model culture system of C6 rat glioma cells was used to test the involvement of cAMP in the regulation of the myelin PLP and MAG genes. The treatment of cells with isoproterenol (10(-5) to 10(-8) M) upregulated the expression of the PLP and MAG genes in a concentration-dependent manner. The mRNA for PLP reached a maximum (sevenfold higher than in control cells) after about 12-24 hr, then declined to approximately fourfold over the control level. The response of MAG gene was delayed by at least 36 hr, and the level of MAG mRNA reached a maximum of approximately 48-fold over the control level on the fourth day in culture. The co-administration of propranolol blocked the effect of isoproterenol, whereas 10(-5) M forskolin simulated the effect of isoproterenol, indicating a role of cAMP in the signal transduction cascades leading to upregulation of the myelin genes. However, the dissimilarity in the timing and the extent of upregulation of the PLP and MAG genes by cAMP-stimulating agents indicate the existence of different intracellular mechanisms for the activation of these two genes. Cycloheximide blocked the stimulatory effect of isoproterenol on both the PLP and MAG genes, indicating that the effect of cAMP on the myelin genes is mediated by protein product(s) of other cAMP-response gene(s).

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“…Several studies showed that MBP synthesis were inhibited by the overexpression of SV40‐Tag at various levels (Tennekoon et al . 1987; Bong et al . 1991; Verity et al .…”

Section: Discussionmentioning

confidence: 99%

Expression of SV40 T antigen gene in the oligodendroglia induced primitive neuroectodermal tumor‐like tumors in the mouse brain

Konishi

Naora

Kimura³

et al. 2004

Congenital Anomalies

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Primitive neuroectodermal tumors (PNET) are classified as the embryonal tumors developed in the brain, except for the cerebellum. Although many studies have been reported, the origin and pathogenesis of PNET are still unclear. In this study, we observed the development of undifferentiated tumors indistinguishable from PNET in the transgenic mice which expressed simian virus 40 T antigen (SV40-Tag) selectively in the oligodendroglia under the control of mouse myelin basic protein gene promoter. These PNET-like tumors reproducibly developed in the brain stem of the founder mice and the transgenic progeny derived from one founder mouse. Oligodendroglia-specific expression of SV40-Tag in these transgenic mice was observed by immunohistochemical analysis. Furthermore, expression of the oligodendroglia-specific marker genes was decreased in the tumors as well as in the transgenic brains. These findings suggested that tumors developed in transgenic mice were indistinguishable from PNET, and one of them showed oligodendroglia-like characteristics. Consequently, this transgenic line is a useful animal model to study the pathogenesis of undifferentiated tumor.

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Differential regulation of myelin gene expression in SV40 T antigen-transfected rat glioma C6 cells

Cited by 16 publications

References 36 publications

Differentiation‐specific demethylation of myelin associated glycoprotein gene in cultured oligodendrocytes

Differentiation‐specific demethylation of myelin associated glycoprotein gene in cultured oligodendrocytes

Cyclic AMP‐induced upregulation of proteolipid protein and myelin associated glycoprotein gene expression in C6 cells

Expression of SV40 T antigen gene in the oligodendroglia induced primitive neuroectodermal tumor‐like tumors in the mouse brain

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