Divalent Metal Transporter 1 Regulates Iron-Mediated ROS and Pancreatic β Cell Fate in Response to Cytokines

Publication: Research - peer-reviewJournal article – Annual report year: 2012

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Divalent Metal Transporter 1 Regulates Iron-Mediated ROS and Pancreatic β Cell Fate in Response to Cytokines. / Hansen, Jakob Bondo; Tonnesen, Morten Fog; Madsen, Andreas Nygaard; Hagedorn, Peter H.; Friberg, Josefine; Grunnet, Lars Groth; Heller, R. Scott; Nielsen, Anja Østergren; Størling, Joachim; Baeyens, Luc; Anker-Kitai, Leeat; Qvortrup, Klaus; Bouwens, Luc; Efrat, Shimon; Aalund, Mogens; Andrews, Nancy C.; Billestrup, Nils; Karlsen, Allan E.; Holst, Birgitte; Pociot, Flemming; Mandrup-Poulsen, Thomas.

In: Cell Metabolism, Vol. 16, No. 4, 2012, p. 449-461.

Publication: Research - peer-reviewJournal article – Annual report year: 2012

Harvard

Hansen, JB, Tonnesen, MF, Madsen, AN, Hagedorn, PH, Friberg, J, Grunnet, LG, Heller, RS, Nielsen, AØ, Størling, J, Baeyens, L, Anker-Kitai, L, Qvortrup, K, Bouwens, L, Efrat, S, Aalund, M, Andrews, NC, Billestrup, N, Karlsen, AE, Holst, B, Pociot, F & Mandrup-Poulsen, T 2012, 'Divalent Metal Transporter 1 Regulates Iron-Mediated ROS and Pancreatic β Cell Fate in Response to Cytokines' Cell Metabolism, vol 16, no. 4, pp. 449-461., 10.1016/j.cmet.2012.09.001

APA

Hansen, J. B., Tonnesen, M. F., Madsen, A. N., Hagedorn, P. H., Friberg, J., Grunnet, L. G., ... Mandrup-Poulsen, T. (2012). Divalent Metal Transporter 1 Regulates Iron-Mediated ROS and Pancreatic β Cell Fate in Response to Cytokines. Cell Metabolism, 16(4), 449-461. 10.1016/j.cmet.2012.09.001

CBE

Hansen JB, Tonnesen MF, Madsen AN, Hagedorn PH, Friberg J, Grunnet LG, Heller RS, Nielsen AØ, Størling J, Baeyens L, Anker-Kitai L, Qvortrup K, Bouwens L, Efrat S, Aalund M, Andrews NC, Billestrup N, Karlsen AE, Holst B, Pociot F, Mandrup-Poulsen T. 2012. Divalent Metal Transporter 1 Regulates Iron-Mediated ROS and Pancreatic β Cell Fate in Response to Cytokines. Cell Metabolism. 16(4):449-461. Available from: 10.1016/j.cmet.2012.09.001

MLA

Vancouver

Author

Hansen, Jakob Bondo; Tonnesen, Morten Fog; Madsen, Andreas Nygaard; Hagedorn, Peter H.; Friberg, Josefine; Grunnet, Lars Groth; Heller, R. Scott; Nielsen, Anja Østergren; Størling, Joachim; Baeyens, Luc; Anker-Kitai, Leeat; Qvortrup, Klaus; Bouwens, Luc; Efrat, Shimon; Aalund, Mogens; Andrews, Nancy C.; Billestrup, Nils; Karlsen, Allan E.; Holst, Birgitte; Pociot, Flemming; Mandrup-Poulsen, Thomas / Divalent Metal Transporter 1 Regulates Iron-Mediated ROS and Pancreatic β Cell Fate in Response to Cytokines.

In: Cell Metabolism, Vol. 16, No. 4, 2012, p. 449-461.

Publication: Research - peer-reviewJournal article – Annual report year: 2012

Bibtex

@article{6800565a6c0b44ac91422c6e0bdf16de,
title = "Divalent Metal Transporter 1 Regulates Iron-Mediated ROS and Pancreatic β Cell Fate in Response to Cytokines",
publisher = "Cell Press",
author = "Hansen, {Jakob Bondo} and Tonnesen, {Morten Fog} and Madsen, {Andreas Nygaard} and Hagedorn, {Peter H.} and Josefine Friberg and Grunnet, {Lars Groth} and Heller, {R. Scott} and Nielsen, {Anja Østergren} and Joachim Størling and Luc Baeyens and Leeat Anker-Kitai and Klaus Qvortrup and Luc Bouwens and Shimon Efrat and Mogens Aalund and Andrews, {Nancy C.} and Nils Billestrup and Karlsen, {Allan E.} and Birgitte Holst and Flemming Pociot and Thomas Mandrup-Poulsen",
year = "2012",
doi = "10.1016/j.cmet.2012.09.001",
volume = "16",
number = "4",
pages = "449--461",
journal = "Cell Metabolism",
issn = "1550-4131",

}

RIS

TY - JOUR

T1 - Divalent Metal Transporter 1 Regulates Iron-Mediated ROS and Pancreatic β Cell Fate in Response to Cytokines

A1 - Hansen,Jakob Bondo

A1 - Tonnesen,Morten Fog

A1 - Madsen,Andreas Nygaard

A1 - Hagedorn,Peter H.

A1 - Friberg,Josefine

A1 - Grunnet,Lars Groth

A1 - Heller,R. Scott

A1 - Nielsen,Anja Østergren

A1 - Størling,Joachim

A1 - Baeyens,Luc

A1 - Anker-Kitai,Leeat

A1 - Qvortrup,Klaus

A1 - Bouwens,Luc

A1 - Efrat,Shimon

A1 - Aalund,Mogens

A1 - Andrews,Nancy C.

A1 - Billestrup,Nils

A1 - Karlsen,Allan E.

A1 - Holst,Birgitte

A1 - Pociot,Flemming

A1 - Mandrup-Poulsen,Thomas

AU - Hansen,Jakob Bondo

AU - Tonnesen,Morten Fog

AU - Madsen,Andreas Nygaard

AU - Hagedorn,Peter H.

AU - Friberg,Josefine

AU - Grunnet,Lars Groth

AU - Heller,R. Scott

AU - Nielsen,Anja Østergren

AU - Størling,Joachim

AU - Baeyens,Luc

AU - Anker-Kitai,Leeat

AU - Qvortrup,Klaus

AU - Bouwens,Luc

AU - Efrat,Shimon

AU - Aalund,Mogens

AU - Andrews,Nancy C.

AU - Billestrup,Nils

AU - Karlsen,Allan E.

AU - Holst,Birgitte

AU - Pociot,Flemming

AU - Mandrup-Poulsen,Thomas

PB - Cell Press

PY - 2012

Y1 - 2012

N2 - Reactive oxygen species (ROS) contribute to target-cell damage in inflammatory and iron-overload diseases. Little is known about iron transport regulation during inflammatory attack. Through a combination of in vitro and in vivo studies, we show that the proinflammatory cytokine IL-1β induces divalent metal transporter 1 (DMT1) expression correlating with increased β cell iron content and ROS production. Iron chelation and siRNA and genetic knockdown of DMT1 expression reduce cytokine-induced ROS formation and cell death. Glucose-stimulated insulin secretion in the absence of cytokines in Dmt1 knockout islets is defective, highlighting a physiological role of iron and ROS in the regulation of insulin secretion. Dmt1 knockout mice are protected against multiple low-dose streptozotocin and high-fat diet-induced glucose intolerance, models of type 1 and type 2 diabetes, respectively. Thus, β cells become prone to ROS-mediated inflammatory damage via aberrant cellular iron metabolism, a finding with potential general cellular implications.

AB - Reactive oxygen species (ROS) contribute to target-cell damage in inflammatory and iron-overload diseases. Little is known about iron transport regulation during inflammatory attack. Through a combination of in vitro and in vivo studies, we show that the proinflammatory cytokine IL-1β induces divalent metal transporter 1 (DMT1) expression correlating with increased β cell iron content and ROS production. Iron chelation and siRNA and genetic knockdown of DMT1 expression reduce cytokine-induced ROS formation and cell death. Glucose-stimulated insulin secretion in the absence of cytokines in Dmt1 knockout islets is defective, highlighting a physiological role of iron and ROS in the regulation of insulin secretion. Dmt1 knockout mice are protected against multiple low-dose streptozotocin and high-fat diet-induced glucose intolerance, models of type 1 and type 2 diabetes, respectively. Thus, β cells become prone to ROS-mediated inflammatory damage via aberrant cellular iron metabolism, a finding with potential general cellular implications.

U2 - 10.1016/j.cmet.2012.09.001

DO - 10.1016/j.cmet.2012.09.001

JO - Cell Metabolism

JF - Cell Metabolism

SN - 1550-4131

IS - 4

VL - 16

SP - 449

EP - 461

ER -