RX871024 reduces NO production but does not protect against pancreatic beta-cell death induced by proinflammatory cytokines.

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

RX871024 reduces NO production but does not protect against pancreatic beta-cell death induced by proinflammatory cytokines. / Zaitseva, Irina I; Sharoyko, Vladimir; Størling, Joachim; Efendic, Suad; Guerin, Christopher; Mandrup-Poulsen, Thomas; Nicotera, Pierluigi; Berggren, Per-Olof; Zaitsev, Sergei V.

In: Biochemical and Biophysical Research Communications, Vol. 347, No. 4, 2006, p. 1121-8.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Zaitseva, II, Sharoyko, V, Størling, J, Efendic, S, Guerin, C, Mandrup-Poulsen, T, Nicotera, P, Berggren, P-O & Zaitsev, SV 2006, 'RX871024 reduces NO production but does not protect against pancreatic beta-cell death induced by proinflammatory cytokines.', Biochemical and Biophysical Research Communications, vol. 347, no. 4, pp. 1121-8. https://doi.org/10.1016/j.bbrc.2006.06.197

APA

Zaitseva, I. I., Sharoyko, V., Størling, J., Efendic, S., Guerin, C., Mandrup-Poulsen, T., Nicotera, P., Berggren, P-O., & Zaitsev, S. V. (2006). RX871024 reduces NO production but does not protect against pancreatic beta-cell death induced by proinflammatory cytokines. Biochemical and Biophysical Research Communications, 347(4), 1121-8. https://doi.org/10.1016/j.bbrc.2006.06.197

Vancouver

Zaitseva II, Sharoyko V, Størling J, Efendic S, Guerin C, Mandrup-Poulsen T et al. RX871024 reduces NO production but does not protect against pancreatic beta-cell death induced by proinflammatory cytokines. Biochemical and Biophysical Research Communications. 2006;347(4):1121-8. https://doi.org/10.1016/j.bbrc.2006.06.197

Author

Zaitseva, Irina I ; Sharoyko, Vladimir ; Størling, Joachim ; Efendic, Suad ; Guerin, Christopher ; Mandrup-Poulsen, Thomas ; Nicotera, Pierluigi ; Berggren, Per-Olof ; Zaitsev, Sergei V. / RX871024 reduces NO production but does not protect against pancreatic beta-cell death induced by proinflammatory cytokines. In: Biochemical and Biophysical Research Communications. 2006 ; Vol. 347, No. 4. pp. 1121-8.

Bibtex

@article{3853ab60acd211ddb538000ea68e967b,
title = "RX871024 reduces NO production but does not protect against pancreatic beta-cell death induced by proinflammatory cytokines.",
abstract = "The imidazoline compound RX871024 reduces IL-1beta-induced NO production thereby protecting against IL-1beta-induced beta-cell apoptosis. The aim of this study was to evaluate whether imidazolines RX871024 and efaroxan protect beta-cells against death in the presence of a combination of the cytokines IL-1beta, IFNgamma, and TNFalpha. To address this issue, experiments involving different methods for detection of cell death, different concentrations of the cytokines, and a variety of conditions of preparation and culturing of ob/ob mouse islets and beta-cells have been carried out. Thoroughly performed experiments have not been able to demonstrate a protective effect of RX871024 and efaroxan on beta-cell death induced by the combination of cytokines. However, the inhibitory effect of RX871024 on NO production in ob/ob mouse islets and beta-cells was still observed in the presence of all three cytokines and correlated with the decrease in p38 MAPK phosphorylation. Conversely, efaroxan did not affect cytokine-induced NO production. Our data indicate that a combination of pro-inflammatory cytokines IL-1beta, IFNgamma, and TNFalpha, conditions modelling those that take place in type 1 diabetes, induces pancreatic beta-cell death that does not directly correlate with NO production and cannot be counteracted with imidazoline compounds.",
author = "Zaitseva, {Irina I} and Vladimir Sharoyko and Joachim St{\o}rling and Suad Efendic and Christopher Guerin and Thomas Mandrup-Poulsen and Pierluigi Nicotera and Per-Olof Berggren and Zaitsev, {Sergei V}",
note = "Keywords: Animals; Benzofurans; Cell Death; Cells, Cultured; Cytokines; Imidazoles; Indoles; Insulin; Insulin-Secreting Cells; Interferon Type II; Interleukin-1; Mice; Mice, Obese; Nitric Oxide; Tumor Necrosis Factor-alpha",
year = "2006",
doi = "10.1016/j.bbrc.2006.06.197",
language = "English",
volume = "347",
pages = "1121--8",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Elsevier",
number = "4",

}

RIS

TY - JOUR

T1 - RX871024 reduces NO production but does not protect against pancreatic beta-cell death induced by proinflammatory cytokines.

AU - Zaitseva, Irina I

AU - Sharoyko, Vladimir

AU - Størling, Joachim

AU - Efendic, Suad

AU - Guerin, Christopher

AU - Mandrup-Poulsen, Thomas

AU - Nicotera, Pierluigi

AU - Berggren, Per-Olof

AU - Zaitsev, Sergei V

N1 - Keywords: Animals; Benzofurans; Cell Death; Cells, Cultured; Cytokines; Imidazoles; Indoles; Insulin; Insulin-Secreting Cells; Interferon Type II; Interleukin-1; Mice; Mice, Obese; Nitric Oxide; Tumor Necrosis Factor-alpha

PY - 2006

Y1 - 2006

N2 - The imidazoline compound RX871024 reduces IL-1beta-induced NO production thereby protecting against IL-1beta-induced beta-cell apoptosis. The aim of this study was to evaluate whether imidazolines RX871024 and efaroxan protect beta-cells against death in the presence of a combination of the cytokines IL-1beta, IFNgamma, and TNFalpha. To address this issue, experiments involving different methods for detection of cell death, different concentrations of the cytokines, and a variety of conditions of preparation and culturing of ob/ob mouse islets and beta-cells have been carried out. Thoroughly performed experiments have not been able to demonstrate a protective effect of RX871024 and efaroxan on beta-cell death induced by the combination of cytokines. However, the inhibitory effect of RX871024 on NO production in ob/ob mouse islets and beta-cells was still observed in the presence of all three cytokines and correlated with the decrease in p38 MAPK phosphorylation. Conversely, efaroxan did not affect cytokine-induced NO production. Our data indicate that a combination of pro-inflammatory cytokines IL-1beta, IFNgamma, and TNFalpha, conditions modelling those that take place in type 1 diabetes, induces pancreatic beta-cell death that does not directly correlate with NO production and cannot be counteracted with imidazoline compounds.

AB - The imidazoline compound RX871024 reduces IL-1beta-induced NO production thereby protecting against IL-1beta-induced beta-cell apoptosis. The aim of this study was to evaluate whether imidazolines RX871024 and efaroxan protect beta-cells against death in the presence of a combination of the cytokines IL-1beta, IFNgamma, and TNFalpha. To address this issue, experiments involving different methods for detection of cell death, different concentrations of the cytokines, and a variety of conditions of preparation and culturing of ob/ob mouse islets and beta-cells have been carried out. Thoroughly performed experiments have not been able to demonstrate a protective effect of RX871024 and efaroxan on beta-cell death induced by the combination of cytokines. However, the inhibitory effect of RX871024 on NO production in ob/ob mouse islets and beta-cells was still observed in the presence of all three cytokines and correlated with the decrease in p38 MAPK phosphorylation. Conversely, efaroxan did not affect cytokine-induced NO production. Our data indicate that a combination of pro-inflammatory cytokines IL-1beta, IFNgamma, and TNFalpha, conditions modelling those that take place in type 1 diabetes, induces pancreatic beta-cell death that does not directly correlate with NO production and cannot be counteracted with imidazoline compounds.

U2 - 10.1016/j.bbrc.2006.06.197

DO - 10.1016/j.bbrc.2006.06.197

M3 - Journal article

C2 - 16870144

VL - 347

SP - 1121

EP - 1128

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 4

ER -

ID: 8465677