Norepinephrine induces glial-specific enzyme activity in cultured plasma glioma cells.

McMorris, F. Arthur

doi:10.1073/pnas.74.10.4501

Cited by 72 publications

(30 citation statements)

References 24 publications

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“…Cholera toxin and forskolin are synergistic in their stimulation of CAMP synthesis in a number of systems, including C,-2B cells (Barovsky et al, 1984), a glioma cell line with some oligodendroglial properties. We have shown previously that dbcAMP induced CNP enzyme activity in C, cells (McMorris, 1977).…”

Section: Discussionmentioning

confidence: 98%

Induction of oligodendrocyte differentiation by activators of adenylate cyclase

Raible

McMorris

1990

J of Neuroscience Research

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Oligodendrocyte differentiation is accelerated by analogs of cyclic AMP (cAMP), such as N6,2-'O-dibutyryladenosine 3',5'-cyclic monophosphate (dbcAMP) or 8-bromo cAMP, in developing rat glial cell cultures (Raible and McMorris, 1989). However, it is not known whether the immature developing oligodendrocytes have G protein-coupled adenylate cyclase capable of generating cAMP, as would be required if development of the cells is normally regulated by endogenous cAMP. In the present study, we demonstrate that the diterpene forskolin, a potent activator of adenylate cyclase, or cholera toxin, which activates adenylate cyclase through G protein modification, can induce a precocious increase in oligodendrocyte number. When both forskolin and cholera toxin are added together, oligodendrocyte differentiation is induced to a level similar to that observed in response to cAMP analogs. These results establish for the first time that modulation of the endogenous cAMP regulatory system alters the schedule of oligodendrocyte differentiation.

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Section: Discussionmentioning

confidence: 98%

Induction of oligodendrocyte differentiation by activators of adenylate cyclase

Raible

McMorris

1990

J of Neuroscience Research

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“…). Moreover, increased CNPase enzymatic activity has been detected by dbcAMP administration in C6 cells and rat oligodendrocytes (McMorris , ). To summarize, neural differentiation was induced by dbcAMP administration in C6 cells, especially astrocyte and oligodendrocyte differentiation.…”

Section: Discussionmentioning

confidence: 99%

Induction of neural differentiation in rat C6 glioma cells with taxol

Chao

Kan

et al. 2015

Brain and Behavior

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BackgroundGlioblastoma is a common and aggressive type of primary brain tumor. Several anticancer drugs affect GBM (glioblastoma multiforme) cells on cell growth and morphology. Taxol is one of the widely used antineoplastic drugs against many types of solid tumors, such as breast, ovarian, and prostate cancers. However, the effect of taxol on GBM cells remains unclear and requires further investigation.MethodsSurvival rate of C6 glioma cells under different taxol concentrations was quantified. To clarify the differentiation patterns of rat C6 glioma cells under taxol challenge, survived glioma cells were characterized by immunocytochemical, molecular biological, and cell biological approaches.ResultsAfter taxol treatment, not only cell death but also morphological changes, including cell elongation, cellular processes thinning, irregular shapes, and fragmented nucleation or micronuclei, occurred in the survived C6 cells. Neural differentiation markers NFL (for neurons), β III‐tubulin (for neurons), GFAP (for astrocytes), and CNPase (for oligodendrocytes) were detected in the taxol‐treated C6 cells. Quantitative analysis suggested a significant increase in the percentage of neural differentiated cells. The results exhibited that taxol may trigger neural differentiation in C6 glioma cells. Increased expression of neural differentiation markers in C6 cells after taxol treatment suggest that some anticancer drugs could be applied to elimination of the malignant cancer cells as well as changing proliferation and differentiation status of tumor cells.

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“…This cell line retains characteristics of undifferentiated gliomas, expresses astrocyte and oligodendrocyte markers, and can be induced to commit to either astrocyte or to the oligodendrocyte lineage, depending on culture conditions (McMorris, 1977;Kumar et al, 1984;Milner et al, 1985). We found a complex interplay between PPARs isoforms in the control of C6 cells differentiation to the oligodendrocyte lineage and also in the regulation of lipid metabolizing enzymes involved in the synthesis of plasmalogens.…”

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confidence: 87%

A PPARs cross‐talk concertedly commits C6 glioma cells to oligodendrocytes and induces enzymes involved in myelin synthesis

Leisewitz

Urrutia

Martinez

et al. 2008

Journal Cellular Physiology

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Peroxisome proliferator activated receptors (PPARs, alpha, beta/delta, gamma) control lipid homeostasis and differentiation in various tissues and tumor cells. PPARbeta and PPARgamma increase oligodendrocyte maturation in glial mixed populations and spinal cord oligodendrocytes, respectively, and PPARbeta is known to modulate the activity of other PPARs. To assess a possible interaction between PPARs in glial cell differentiation we used the undifferentiated C6 glioma cell line as model. These cells express all three PPARs, but only PPARgamma shows transcriptional activity in agonist-based reporter gene assay. Agonist-activated PPARgamma up-regulates oligodendrocyte markers, down-regulates an astrocyte marker, and increases alkyl-dihydroxyacetone phosphate synthase, enzyme involved in the synthesis of myelin-rich plasmalogens. Similar effects are induced in PPARgamma overexpressing cells, which in addition show PPARbeta up-regulation. PPARbeta or PPARalpha agonists show no effect. Nevertheless, PPARbeta overexpression up-regulates PPARgamma and commits C6 cells to oligodendrocytes; effect that is abrogated by a PPARgamma antagonist or PPARgamma interference RNA. Moreover, PPARbeta overexpression also induces PPARalpha and its target genes, including acyl-CoA oxidase, enzyme involved in very long chain fatty acid recycling, and in the synthesis of myelin components such as docosahexaenoic acid. These results indicate for the first time, that PPARs concertedly cooperate in C6 glioma cell differentiation to oligodendrocytes. Further, they suggest that active PPARbeta might be essential for increasing oligodendrocyte distinctive markers and enzymes required for myelin synthesis in C6 glioma cells through up-regulation of PPARgamma and PPARalpha.

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Norepinephrine induces glial-specific enzyme activity in cultured plasma glioma cells.

Cited by 72 publications

References 24 publications

Induction of oligodendrocyte differentiation by activators of adenylate cyclase

Induction of oligodendrocyte differentiation by activators of adenylate cyclase

Induction of neural differentiation in rat C6 glioma cells with taxol

A PPARs cross‐talk concertedly commits C6 glioma cells to oligodendrocytes and induces enzymes involved in myelin synthesis

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