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Interferon-gamma alone triggers the production of nitric oxide from serum-starved BNL CL.2, murine embryonic liver cells.
Immunol Invest 1999 Mar-May; 28(2-3):149-63II

Abstract

A previous study has demonstrated that both interferon-gamma (IFN-gamma) and lipopolysaccharide (LPS) were needed to induce the production of nitric oxide (NO) in BNL CL.2 cells, murine embryonic liver cells. We here demonstrate that when BNL CL.2 cells were cultured with serum-free medium, they were induced to produce NO by the stimulation of IFN-gamma alone. BNL CL.2 cells were cultured with serum-free or serum-containing medium for 1-3 days and then stimulated to synthesize NO by IFN-gamma. Surprisingly, only serum-starved cells showed significant amount of nitrite accumulation and iNOS protein expression in response to IFN-gamma in dose- and time-dependent manners, but serum-supplied cells did not. When the cells were stimulated with IFN-gamma, tumor necrosis factor-alpha (TNF-alpha), or LPS in combinations, only the combination of IFN-gamma and LPS produced more NO than that produced by IFN-gamma alone. The production of NO by the cells stimulated with IFN-gamma or IFN-gamma plus LPS was blocked by the addition of N(G)-monomethyl-L-arginine (N(G)MMA), a NO synthesis inhibitor. To address the intracellular signal pathway responsible for the production of NO by the cells stimulated with IFN-gamma aloneor IFN-gamma plus LPS, we examined the effects of several protein kinase inhibitors on the production of NO from the cells. The production of NO was significantly inhibited by protein tyrosine kinase (PTK) inhibitors, genistein and herbimycin A, but not by protein kinase A or C inhibitors. These results suggest that the deprivation of serum from BNL CL.2 cell culture medium might prime the cells to induce NO synthesis when the cells are triggered by IFN-gamma and the involvement of PTK signal transduction pathway in the expression of inducible NO synthase gene in murine hepatoma cells.

Authors+Show Affiliations

Department of Microbiology and Immunology, Wonkwang University School of Medicine, Medicinal Resources Research Center of Wonkwang University, Iksan, Chonbug, Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10484680

Citation

Pae, H O., et al. "Interferon-gamma Alone Triggers the Production of Nitric Oxide From Serum-starved BNL CL.2, Murine Embryonic Liver Cells." Immunological Investigations, vol. 28, no. 2-3, 1999, pp. 149-63.
Pae HO, Yoo JC, Choi BM, et al. Interferon-gamma alone triggers the production of nitric oxide from serum-starved BNL CL.2, murine embryonic liver cells. Immunol Invest. 1999;28(2-3):149-63.
Pae, H. O., Yoo, J. C., Choi, B. M., Paik, S. G., Kim, Y. H., Jin, H. S., & Chung, H. T. (1999). Interferon-gamma alone triggers the production of nitric oxide from serum-starved BNL CL.2, murine embryonic liver cells. Immunological Investigations, 28(2-3), pp. 149-63.
Pae HO, et al. Interferon-gamma Alone Triggers the Production of Nitric Oxide From Serum-starved BNL CL.2, Murine Embryonic Liver Cells. Immunol Invest. 1999;28(2-3):149-63. PubMed PMID: 10484680.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Interferon-gamma alone triggers the production of nitric oxide from serum-starved BNL CL.2, murine embryonic liver cells. AU - Pae,H O, AU - Yoo,J C, AU - Choi,B M, AU - Paik,S G, AU - Kim,Y H, AU - Jin,H S, AU - Chung,H T, PY - 1999/9/15/pubmed PY - 1999/9/15/medline PY - 1999/9/15/entrez SP - 149 EP - 63 JF - Immunological investigations JO - Immunol. Invest. VL - 28 IS - 2-3 N2 - A previous study has demonstrated that both interferon-gamma (IFN-gamma) and lipopolysaccharide (LPS) were needed to induce the production of nitric oxide (NO) in BNL CL.2 cells, murine embryonic liver cells. We here demonstrate that when BNL CL.2 cells were cultured with serum-free medium, they were induced to produce NO by the stimulation of IFN-gamma alone. BNL CL.2 cells were cultured with serum-free or serum-containing medium for 1-3 days and then stimulated to synthesize NO by IFN-gamma. Surprisingly, only serum-starved cells showed significant amount of nitrite accumulation and iNOS protein expression in response to IFN-gamma in dose- and time-dependent manners, but serum-supplied cells did not. When the cells were stimulated with IFN-gamma, tumor necrosis factor-alpha (TNF-alpha), or LPS in combinations, only the combination of IFN-gamma and LPS produced more NO than that produced by IFN-gamma alone. The production of NO by the cells stimulated with IFN-gamma or IFN-gamma plus LPS was blocked by the addition of N(G)-monomethyl-L-arginine (N(G)MMA), a NO synthesis inhibitor. To address the intracellular signal pathway responsible for the production of NO by the cells stimulated with IFN-gamma aloneor IFN-gamma plus LPS, we examined the effects of several protein kinase inhibitors on the production of NO from the cells. The production of NO was significantly inhibited by protein tyrosine kinase (PTK) inhibitors, genistein and herbimycin A, but not by protein kinase A or C inhibitors. These results suggest that the deprivation of serum from BNL CL.2 cell culture medium might prime the cells to induce NO synthesis when the cells are triggered by IFN-gamma and the involvement of PTK signal transduction pathway in the expression of inducible NO synthase gene in murine hepatoma cells. SN - 0882-0139 UR - https://www.unboundmedicine.com/medline/citation/10484680/Interferon_gamma_alone_triggers_the_production_of_nitric_oxide_from_serum_starved_BNL_CL_2_murine_embryonic_liver_cells_ DB - PRIME DP - Unbound Medicine ER -