Nitric oxide contributes to cytokine-induced apoptosis in pancreatic beta cells via potentiation of JNK activity and inhibition of Akt

J Størling; J Binzer; Annica Andersson; R A Züllig; M Tonnesen; René Lehmann Pulz Knudsen; G A Spinas; S Sandler; N Billestrup; Thomas Mandrup-Poulsen

doi:10.1007/s00125-005-1912-2

Nitric oxide contributes to cytokine-induced apoptosis in pancreatic beta cells via potentiation of JNK activity and inhibition of Akt

J Størling, J Binzer, Annica Andersson, R A Züllig, M Tonnesen, René Lehmann Pulz Knudsen, G A Spinas, S Sandler, N Billestrup, Thomas Mandrup-Poulsen

Endocrinology and Metabolism

105 Citations (Scopus)

Abstract

Pro-inflammatory cytokines cause beta cell secretory dysfunction and apoptosis--a process implicated in the pathogenesis of type 1 diabetes. Cytokines induce the expression of inducible nitric oxide (NO) synthase (iNOS) leading to NO production. NO contributes to cytokine-induced apoptosis, but the underlying mechanisms are unclear. The aim of this study was to investigate whether NO modulates signalling via mitogen-activated protein kinases (MAPKs) and Akt.

Original language	English
Journal	Diabetologia
Volume	48
Issue number	10
Pages (from-to)	2039-50
Number of pages	12
ISSN	0012-186X
DOIs	https://doi.org/10.1007/s00125-005-1912-2
Publication status	Published - 1 Oct 2005

Keywords

Animals
Apoptosis
Blotting, Western
Cell Separation
Cells, Cultured
Cytokines
Dose-Response Relationship, Drug
Enzyme Activation
Enzyme Inhibitors
Humans
Insulin
Insulin-Secreting Cells
MAP Kinase Kinase 4
Mice
Mitogen-Activated Protein Kinases
NG-Nitroarginine Methyl Ester
Nitric Oxide
Nitric Oxide Donors
Nitric Oxide Synthase Type II
Oncogene Protein v-akt
S-Nitroso-N-Acetylpenicillamine
Signal Transduction
p38 Mitogen-Activated Protein Kinases

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1007/s00125-005-1912-2

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Størling, J., Binzer, J., Andersson, A., Züllig, R. A., Tonnesen, M., Knudsen, R. L. P., Spinas, G. A., Sandler, S., Billestrup, N., & Mandrup-Poulsen, T. (2005). Nitric oxide contributes to cytokine-induced apoptosis in pancreatic beta cells via potentiation of JNK activity and inhibition of Akt. Diabetologia, 48(10), 2039-50. https://doi.org/10.1007/s00125-005-1912-2

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title = "Nitric oxide contributes to cytokine-induced apoptosis in pancreatic beta cells via potentiation of JNK activity and inhibition of Akt",

abstract = "Pro-inflammatory cytokines cause beta cell secretory dysfunction and apoptosis--a process implicated in the pathogenesis of type 1 diabetes. Cytokines induce the expression of inducible nitric oxide (NO) synthase (iNOS) leading to NO production. NO contributes to cytokine-induced apoptosis, but the underlying mechanisms are unclear. The aim of this study was to investigate whether NO modulates signalling via mitogen-activated protein kinases (MAPKs) and Akt.",

keywords = "Animals, Apoptosis, Blotting, Western, Cell Separation, Cells, Cultured, Cytokines, Dose-Response Relationship, Drug, Enzyme Activation, Enzyme Inhibitors, Humans, Insulin, Insulin-Secreting Cells, MAP Kinase Kinase 4, Mice, Mitogen-Activated Protein Kinases, NG-Nitroarginine Methyl Ester, Nitric Oxide, Nitric Oxide Donors, Nitric Oxide Synthase Type II, Oncogene Protein v-akt, S-Nitroso-N-Acetylpenicillamine, Signal Transduction, p38 Mitogen-Activated Protein Kinases",

author = "J St{\o}rling and J Binzer and Annica Andersson and Z{\"u}llig, {R A} and M Tonnesen and Knudsen, {Ren{\'e} Lehmann Pulz} and Spinas, {G A} and S Sandler and N Billestrup and Thomas Mandrup-Poulsen",

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doi = "10.1007/s00125-005-1912-2",

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TY - JOUR

T1 - Nitric oxide contributes to cytokine-induced apoptosis in pancreatic beta cells via potentiation of JNK activity and inhibition of Akt

AU - Størling, J

AU - Binzer, J

AU - Andersson, Annica

AU - Züllig, R A

AU - Tonnesen, M

AU - Knudsen, René Lehmann Pulz

AU - Spinas, G A

AU - Sandler, S

AU - Billestrup, N

AU - Mandrup-Poulsen, Thomas

PY - 2005/10/1

Y1 - 2005/10/1

N2 - Pro-inflammatory cytokines cause beta cell secretory dysfunction and apoptosis--a process implicated in the pathogenesis of type 1 diabetes. Cytokines induce the expression of inducible nitric oxide (NO) synthase (iNOS) leading to NO production. NO contributes to cytokine-induced apoptosis, but the underlying mechanisms are unclear. The aim of this study was to investigate whether NO modulates signalling via mitogen-activated protein kinases (MAPKs) and Akt.

AB - Pro-inflammatory cytokines cause beta cell secretory dysfunction and apoptosis--a process implicated in the pathogenesis of type 1 diabetes. Cytokines induce the expression of inducible nitric oxide (NO) synthase (iNOS) leading to NO production. NO contributes to cytokine-induced apoptosis, but the underlying mechanisms are unclear. The aim of this study was to investigate whether NO modulates signalling via mitogen-activated protein kinases (MAPKs) and Akt.

KW - Animals

KW - Apoptosis

KW - Blotting, Western

KW - Cell Separation

KW - Cells, Cultured

KW - Cytokines

KW - Dose-Response Relationship, Drug

KW - Enzyme Activation

KW - Enzyme Inhibitors

KW - Humans

KW - Insulin

KW - Insulin-Secreting Cells

KW - MAP Kinase Kinase 4

KW - Mice

KW - Mitogen-Activated Protein Kinases

KW - NG-Nitroarginine Methyl Ester

KW - Nitric Oxide

KW - Nitric Oxide Donors

KW - Nitric Oxide Synthase Type II

KW - Oncogene Protein v-akt

KW - S-Nitroso-N-Acetylpenicillamine

KW - Signal Transduction

KW - p38 Mitogen-Activated Protein Kinases

U2 - 10.1007/s00125-005-1912-2

DO - 10.1007/s00125-005-1912-2

M3 - Journal article

C2 - 16132952

SN - 0012-186X

VL - 48

SP - 2039

EP - 2050

JO - Diabetologia

JF - Diabetologia

IS - 10

ER -

Nitric oxide contributes to cytokine-induced apoptosis in pancreatic beta cells via potentiation of JNK activity and inhibition of Akt

Abstract

Keywords

UN SDGs

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