IL-1 beta-induced chemokine and Fas expression are inhibited by suppressor of cytokine signalling-3 in insulin-producing cells

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Standard

IL-1 beta-induced chemokine and Fas expression are inhibited by suppressor of cytokine signalling-3 in insulin-producing cells. / Jacobsen, M.L.B.; Ronn, S.G.; Bruun, C.; Larsen, C.M.; Eizirik, D.L.; Mandrup-Poulsen, T.; Billestrup, N.

I: Diabetologia, Bind 52, Nr. 2, 2009, s. 281-288.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Jacobsen, MLB, Ronn, SG, Bruun, C, Larsen, CM, Eizirik, DL, Mandrup-Poulsen, T & Billestrup, N 2009, 'IL-1 beta-induced chemokine and Fas expression are inhibited by suppressor of cytokine signalling-3 in insulin-producing cells', Diabetologia, bind 52, nr. 2, s. 281-288.

APA

Jacobsen, M. L. B., Ronn, S. G., Bruun, C., Larsen, C. M., Eizirik, D. L., Mandrup-Poulsen, T., & Billestrup, N. (2009). IL-1 beta-induced chemokine and Fas expression are inhibited by suppressor of cytokine signalling-3 in insulin-producing cells. Diabetologia, 52(2), 281-288.

Vancouver

Jacobsen MLB, Ronn SG, Bruun C, Larsen CM, Eizirik DL, Mandrup-Poulsen T o.a. IL-1 beta-induced chemokine and Fas expression are inhibited by suppressor of cytokine signalling-3 in insulin-producing cells. Diabetologia. 2009;52(2):281-288.

Author

Jacobsen, M.L.B. ; Ronn, S.G. ; Bruun, C. ; Larsen, C.M. ; Eizirik, D.L. ; Mandrup-Poulsen, T. ; Billestrup, N. / IL-1 beta-induced chemokine and Fas expression are inhibited by suppressor of cytokine signalling-3 in insulin-producing cells. I: Diabetologia. 2009 ; Bind 52, Nr. 2. s. 281-288.

Bibtex

@article{4b9b2ed089c811df928f000ea68e967b,
title = "IL-1 beta-induced chemokine and Fas expression are inhibited by suppressor of cytokine signalling-3 in insulin-producing cells",
abstract = "Chemokines recruit activated immune cells to sites of inflammation and are important mediators of insulitis. Activation of the pro-apoptotic receptor Fas leads to apoptosis-mediated death of the Fas-expressing cell. The pro-inflammatory cytokines IL-1 beta and IFN-gamma regulate the transcription of genes encoding the Fas receptor and several chemokines. We have previously shown that suppressor of cytokine signalling (SOCS)-3 inhibits IL-1 beta- and IFN-gamma-induced nitric oxide production in a beta cell line. The aim of this study was to investigate whether SOCS-3 can influence cytokine-induced Fas and chemokine expression in beta cells. Using a beta cell line with inducible Socs3 expression or primary neonatal rat islet cells transduced with a Socs3-encoding adenovirus, we employed real-time RT-PCR analysis to investigate whether SOCS-3 affects cytokine-induced chemokine and Fas mRNA expression. The ability of SOCS-3 to influence the activity of cytokine-responsive Fas and Mcp-1 (also known as Ccl2) promoters was measured by reporter analysis. IL-1 beta induced a time-dependent increase in Mcp-1 and Mip-2 (also known as Cxcl2) mRNA expression after 6 h of stimulation in insulinoma (INS)-1 and neonatal rat islet cells. This induction was inhibited when Socs3 was expressed in the cells. In INS-1 cells, IL-1 beta + IFN-gamma induced a tenfold and eightfold increase of Fas mRNA expression after 6 and 24 h, respectively. This induction was inhibited at both time-points when expression of Socs3 was induced. In promoter studies SOCS-3 significantly inhibited the cytokine-induced activity of Mcp-1 and Fas promoter constructs. SOCS-3 inhibits the expression of cytokine-induced chemokine and death-receptor Fas mRNA Udgivelsesdato: 2009/2",
author = "M.L.B. Jacobsen and S.G. Ronn and C. Bruun and C.M. Larsen and D.L. Eizirik and T. Mandrup-Poulsen and N. Billestrup",
note = "Times Cited: 3ArticleEnglishBillestrup, NSteno Diabet Ctr, Niels Steensens Vej 6,NSK2-02, DK-2820 Gentofte, DenmarkCited References Count: 40393YASPRINGER233 SPRING ST, NEW YORK, NY 10013 USANEW YORK",
year = "2009",
language = "English",
volume = "52",
pages = "281--288",
journal = "Diabetologia",
issn = "0012-186X",
publisher = "Springer",
number = "2",

}

RIS

TY - JOUR

T1 - IL-1 beta-induced chemokine and Fas expression are inhibited by suppressor of cytokine signalling-3 in insulin-producing cells

AU - Jacobsen, M.L.B.

AU - Ronn, S.G.

AU - Bruun, C.

AU - Larsen, C.M.

AU - Eizirik, D.L.

AU - Mandrup-Poulsen, T.

AU - Billestrup, N.

N1 - Times Cited: 3ArticleEnglishBillestrup, NSteno Diabet Ctr, Niels Steensens Vej 6,NSK2-02, DK-2820 Gentofte, DenmarkCited References Count: 40393YASPRINGER233 SPRING ST, NEW YORK, NY 10013 USANEW YORK

PY - 2009

Y1 - 2009

N2 - Chemokines recruit activated immune cells to sites of inflammation and are important mediators of insulitis. Activation of the pro-apoptotic receptor Fas leads to apoptosis-mediated death of the Fas-expressing cell. The pro-inflammatory cytokines IL-1 beta and IFN-gamma regulate the transcription of genes encoding the Fas receptor and several chemokines. We have previously shown that suppressor of cytokine signalling (SOCS)-3 inhibits IL-1 beta- and IFN-gamma-induced nitric oxide production in a beta cell line. The aim of this study was to investigate whether SOCS-3 can influence cytokine-induced Fas and chemokine expression in beta cells. Using a beta cell line with inducible Socs3 expression or primary neonatal rat islet cells transduced with a Socs3-encoding adenovirus, we employed real-time RT-PCR analysis to investigate whether SOCS-3 affects cytokine-induced chemokine and Fas mRNA expression. The ability of SOCS-3 to influence the activity of cytokine-responsive Fas and Mcp-1 (also known as Ccl2) promoters was measured by reporter analysis. IL-1 beta induced a time-dependent increase in Mcp-1 and Mip-2 (also known as Cxcl2) mRNA expression after 6 h of stimulation in insulinoma (INS)-1 and neonatal rat islet cells. This induction was inhibited when Socs3 was expressed in the cells. In INS-1 cells, IL-1 beta + IFN-gamma induced a tenfold and eightfold increase of Fas mRNA expression after 6 and 24 h, respectively. This induction was inhibited at both time-points when expression of Socs3 was induced. In promoter studies SOCS-3 significantly inhibited the cytokine-induced activity of Mcp-1 and Fas promoter constructs. SOCS-3 inhibits the expression of cytokine-induced chemokine and death-receptor Fas mRNA Udgivelsesdato: 2009/2

AB - Chemokines recruit activated immune cells to sites of inflammation and are important mediators of insulitis. Activation of the pro-apoptotic receptor Fas leads to apoptosis-mediated death of the Fas-expressing cell. The pro-inflammatory cytokines IL-1 beta and IFN-gamma regulate the transcription of genes encoding the Fas receptor and several chemokines. We have previously shown that suppressor of cytokine signalling (SOCS)-3 inhibits IL-1 beta- and IFN-gamma-induced nitric oxide production in a beta cell line. The aim of this study was to investigate whether SOCS-3 can influence cytokine-induced Fas and chemokine expression in beta cells. Using a beta cell line with inducible Socs3 expression or primary neonatal rat islet cells transduced with a Socs3-encoding adenovirus, we employed real-time RT-PCR analysis to investigate whether SOCS-3 affects cytokine-induced chemokine and Fas mRNA expression. The ability of SOCS-3 to influence the activity of cytokine-responsive Fas and Mcp-1 (also known as Ccl2) promoters was measured by reporter analysis. IL-1 beta induced a time-dependent increase in Mcp-1 and Mip-2 (also known as Cxcl2) mRNA expression after 6 h of stimulation in insulinoma (INS)-1 and neonatal rat islet cells. This induction was inhibited when Socs3 was expressed in the cells. In INS-1 cells, IL-1 beta + IFN-gamma induced a tenfold and eightfold increase of Fas mRNA expression after 6 and 24 h, respectively. This induction was inhibited at both time-points when expression of Socs3 was induced. In promoter studies SOCS-3 significantly inhibited the cytokine-induced activity of Mcp-1 and Fas promoter constructs. SOCS-3 inhibits the expression of cytokine-induced chemokine and death-receptor Fas mRNA Udgivelsesdato: 2009/2

M3 - Journal article

VL - 52

SP - 281

EP - 288

JO - Diabetologia

JF - Diabetologia

SN - 0012-186X

IS - 2

ER -

ID: 20688541