Tetraethylammonium, a K+ channel blocker, inhibits interferon-γ-induced major histocompatibility class II antigen (Ia) expression and DNA synthesis in rat astrocytes

Ohira, Kiyoshi; Vayuvegula, Bharathi; Murakami, Masaru; Gollapudi, Sastry; Frohman, Elliott; Noort, Stanley van den; Gupta, Sudhir

doi:10.1016/0165-5728(91)90085-l

Cited by 10 publications

(6 citation statements)

References 26 publications

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“…2). This is similar to the dose used to elicit an effect on factor H expression in other cell types and is in the range seen for other effects induced by IFN-, including induction of class II genes [37], intercellular adhesion molecule-1 [38], C1q [39], carcinoembryonic antigen, biliary glycoprotein and non-specific cross-reacting antigen [40]. The increase in mRNA also resulted in increased secretion of factor H protein into the medium.…”

Section: Discussionmentioning

confidence: 64%

Regulation of Expression of the Complement Factor H Gene in a Murine Liver Cell Line by Interferon‐γ

Vik

1996

Scand J Immunol

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Factor H is a regulatory protein of the alternative pathway of complement activation that is synthesized mainly in the liver. The authors used the +/+ Li murine liver cell line as a model for examining its regulation. When +/+ Li cells were incubated with IFN-gamma, the levels of factor H mRNA increased in a dose-dependent manner, achieving a maximal response at a concentration of 50-100 units/ml. The increase in factor H mRNA levels was paralleled by an increase in factor H secretion. The kinetics of induction of factor H mRNA were slow, with the response reaching near maximal levels at 24 h. The increase in factor H mRNA by IFN-gamma was dependent on protein synthesis, as cycloheximide abolished the response. The presence of IFN-gamma was required for the entire incubation period in order to produce a maximal response. The luciferase system was used in an attempt to identify an interferon-responsive element. Luciferase constructs containing from 807 to 236 bp of upstream sequence responded to IFN-gamma with a twofold induction of luciferase activity, whereas a construct containing 83 bp of 5' sequence did not. Thus, IFN-gamma stimulates factor H mRNA transcription through a protein intermediary that interacts with the promoter between positions -83 and -236.

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Section: Discussionmentioning

confidence: 64%

Regulation of Expression of the Complement Factor H Gene in a Murine Liver Cell Line by Interferon‐γ

Vik

1996

Scand J Immunol

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“…1). This is similar to the dose used to elicit an effect on factor H expression in other cell types, such as murine þ / þ li cell line [32], and is in the range seen for other effects induced by IFN-␥, including induction of class II genes [34], intercellular adhesion molecule-1 [35], C1q [36], carcinoembryonic antigen, biliary glycoprotein and non-specific cross-reacting antigens [37].…”

Section: Discussionmentioning

confidence: 99%

“…Determination of factor H mRNA half-life in Hep3b cells. The half-life of mRNA in IFN-␥-treated cells was measured following the inhibition of transcription with actinomycin D (5 g/ml: Sigma, St Louis, MO, USA) [34], which binds to DNA and blocks the movement of RNA polymerase, preventing RNA synthesis. The cells were incubated with IFN-␥ for 24 h before the addition of actinomycin D, and total cellular RNA was prepared at timed intervals after the addition of actinomycin D, analysed by RT-PCR.…”

Section: Methodsmentioning

confidence: 99%

Regulation of Complement Factor H in a Human Liver Cell Line by Interferon‐γ

Luo

1999

Scand J Immunol

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Factor H is a regulatory protein of the alternative pathway of complement activation. The liver is the major site of synthesis. We have used the Hep3b human liver cell line as a model for examining its regulation by interferon-gamma (IFN-gamma). The maximal response was achieved at 50 U/ml of IFN-gamma. An increase in H mRNA was observed as early as 2 h after addition of IFN-gamma; the response peaked at 24 h. The half-life of H mRNA in the presence of IFN-gamma was 3.8 +/- 0.8 h. The increase in H mRNA by IFN-gamma was partly dependent on protein synthesis, as cycloheximide (CHX) reduced the response by 40% and the level of H mRNA decreased in a dose-dependent manner with increasing concentrations of CHX. Phosphorylation events were also important in this induction because the kinase inhibitors staurosporine and genistein inhibited the induction of H mRNA by 88% and 68%, respectively. The induction could be inhibited completely when Hep3b cells were treated with CHX and staurosporine. Thus induction of factor H by IFN-gamma apparently involves two factors. One is likely to be Stat1alpha and the other is a CHX-sensitive protein.

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“…Ohira et al [40] have recently reported that while rat and mouse y-IFN induced class II MHC antigen on rat astrocytes in vitro, human y-IFN could not induce these molecules. While there are differences in glycosylation between the rat and mouse y-IFN it did not seem to be important in induction of MHC class I antigens.…”

Section: Discussionmentioning

confidence: 99%

Differences in the Capacity of Gamma-Interferons from Different Species to Induce Class I and II Major Histocompatibility Complex Antigens on Neonatal Rat Schwann Cells in vitro

Lisak

Bealmear

1992

Pathobiology

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We compared the capacity of unfractionated cytokines and recombinant γ-interferons (γ-IFN) to induce major histocompatibility (MHC) antigens on neonatal rat Schwann cells and endoneurial fibroblasts in vitro. Rat and mouse γ-IFN were capable of induction of both class I and class II MHC antigens on both cell types although rat γ-IFN was more potent than that of mouse. Human γ-IFN failed to induce MHC class I or class II on either cell type. Unfractionated cytokines from the different species also differed in their capacity to induce MHC antigens. Differences in species of origin of cytokine mixtures as well as in individual cytokines, such as γ-IFN need to be considered in studies of MHC induction. The presence of MHC class I and class II antigens on Schwann cells could render them susceptible to cytotoxic reactions and allow for the presentation of antigen, respectively.

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Tetraethylammonium, a K+ channel blocker, inhibits interferon-γ-induced major histocompatibility class II antigen (Ia) expression and DNA synthesis in rat astrocytes

Cited by 10 publications

References 26 publications

Regulation of Expression of the Complement Factor H Gene in a Murine Liver Cell Line by Interferon‐γ

Regulation of Expression of the Complement Factor H Gene in a Murine Liver Cell Line by Interferon‐γ

Regulation of Complement Factor H in a Human Liver Cell Line by Interferon‐γ

Differences in the Capacity of Gamma-Interferons from Different Species to Induce Class I and II Major Histocompatibility Complex Antigens on Neonatal Rat Schwann Cells in vitro

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