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Gremlin-1 is an inhibitor of macrophage migration inhibitory factor and attenuates atherosclerotic plaque growth in ApoE-/- mice

Publikation: Beiträge in Zeitschriften › Zeitschriftenaufsätze › Forschung › begutachtet

Standard

Gremlin-1 is an inhibitor of macrophage migration inhibitory factor and attenuates atherosclerotic plaque growth in ApoE-/- mice. / Müller, Iris; Schönberger, Tanja; Schneider, Martina et al.

in: The Journal of Biological Chemistry, Jahrgang 288, Nr. 44, 01.11.2013, S. 31635-31645.

Publikation: Beiträge in Zeitschriften › Zeitschriftenaufsätze › Forschung › begutachtet

Harvard

Müller, I, Schönberger, T, Schneider, M, Borst, O, Ziegler, M, Seizer, P, Leder, C, Müller, K, Lang, M, Appenzeller, F, Lunov, O, Büchele, B, Fahrleitner, M, Olbrich, M, Langer, H, Geisler, T, Lang, F, Chatterjee, M, de Boer, JF, Tietge, UJ, Bernhagen, J, Simmet, T & Gawaz, M 2013, 'Gremlin-1 is an inhibitor of macrophage migration inhibitory factor and attenuates atherosclerotic plaque growth in ApoE-/- mice', The Journal of Biological Chemistry, Jg. 288, Nr. 44, S. 31635-31645. https://doi.org/10.1074/jbc.M113.477745

APA

Müller, I., Schönberger, T., Schneider, M., Borst, O., Ziegler, M., Seizer, P., Leder, C., Müller, K., Lang, M., Appenzeller, F., Lunov, O., Büchele, B., Fahrleitner, M., Olbrich, M., Langer, H., Geisler, T., Lang, F., Chatterjee, M., de Boer, J. F., ... Gawaz, M. (2013). Gremlin-1 is an inhibitor of macrophage migration inhibitory factor and attenuates atherosclerotic plaque growth in ApoE-/- mice. The Journal of Biological Chemistry, 288(44), 31635-31645. https://doi.org/10.1074/jbc.M113.477745

Vancouver

Müller I, Schönberger T, Schneider M, Borst O, Ziegler M, Seizer P et al. Gremlin-1 is an inhibitor of macrophage migration inhibitory factor and attenuates atherosclerotic plaque growth in ApoE-/- mice. The Journal of Biological Chemistry. 2013 Nov 1;288(44):31635-31645. doi: 10.1074/jbc.M113.477745

Bibtex

@article{ceba76f325964133b399b3898e120529,
title = "Gremlin-1 is an inhibitor of macrophage migration inhibitory factor and attenuates atherosclerotic plaque growth in ApoE-/- mice",
abstract = "Monocyte infiltration and macrophage formation are pivotal steps in atherosclerosis and plaque vulnerability. Gremlin-1/Drm is crucial in embryo-/organogenesis and has been shown to be expressed in the adult organism at sites of arterial injury and to inhibit monocyte migration. The purpose of the present study was to evaluate and characterize the role of Gremlin-1 in atherosclerosis. Here we report that Gremlin-1 is highly expressed primarily by monocytes/macrophages in aortic atherosclerotic lesions of ApoE -/- mice and is secreted from activated monocytes and during macrophage development in vitro. Gremlin-1 reduces macrophage formation by inhibiting macrophage migration inhibitory factor (MIF), a cytokine critically involved in atherosclerotic plaque progression and vulnerability. Gremlin-1 binds with high affinity to MIF (K D = 54 nM), as evidenced by surface plasmon resonance analysis and co-immunoprecipitation, and reduces MIF-induced release of TNF-α from macrophages. Treatment of ApoE -/- mice with a dimeric recombinant fusion protein, mGremlin1-Fc, but not with equimolar control Fc or inactivated mGremlin1-Fc, reduced TNF-α expression, the content of monocytes/macrophages of atherosclerotic lesions, and attenuated atheroprogression. The present data disclose that Gremlin-1 is an endogenous antagonist of MIF and define a role for Gremlin-1/MIF interaction in atherosclerosis.",
keywords = "Biology, Atherosclerosis, Chemokines, Inflammation, Monocytes, Vascular biology, Atherosclerosis, Chemokiness, Inflammation, Monocytes, Vascular biology, Sustainability Science",
author = "Iris M{\"u}ller and Tanja Sch{\"o}nberger and Martina Schneider and Oliver Borst and Melanie Ziegler and Peter Seizer and Christoph Leder and Karin M{\"u}ller and Michael Lang and Florian Appenzeller and Oleg Lunov and Berthold B{\"u}chele and Manuela Fahrleitner and Marcus Olbrich and Harald Langer and Tobias Geisler and Florian Lang and Madhumita Chatterjee and {de Boer}, {Jan Freark} and Tietge, {Uwe J} and J{\"u}rgen Bernhagen and Thomas Simmet and Meinrad Gawaz",
note = "DFG Funding: MU 2928/2-1",
year = "2013",
month = nov,
day = "1",
doi = "10.1074/jbc.M113.477745",
language = "English",
volume = "288",
pages = "31635--31645",
journal = "Journal of Biological Chemistry",
issn = "0021-9258",
publisher = "American Society for Biochemistry and Molecular Biology Inc.",
number = "44",

}

RIS

TY - JOUR

T1 - Gremlin-1 is an inhibitor of macrophage migration inhibitory factor and attenuates atherosclerotic plaque growth in ApoE-/- mice

AU - Müller, Iris

AU - Schönberger, Tanja

AU - Schneider, Martina

AU - Borst, Oliver

AU - Ziegler, Melanie

AU - Seizer, Peter

AU - Leder, Christoph

AU - Müller, Karin

AU - Lang, Michael

AU - Appenzeller, Florian

AU - Lunov, Oleg

AU - Büchele, Berthold

AU - Fahrleitner, Manuela

AU - Olbrich, Marcus

AU - Langer, Harald

AU - Geisler, Tobias

AU - Lang, Florian

AU - Chatterjee, Madhumita

AU - de Boer, Jan Freark

AU - Tietge, Uwe J

AU - Bernhagen, Jürgen

AU - Simmet, Thomas

AU - Gawaz, Meinrad

N1 - DFG Funding: MU 2928/2-1

PY - 2013/11/1

Y1 - 2013/11/1

N2 - Monocyte infiltration and macrophage formation are pivotal steps in atherosclerosis and plaque vulnerability. Gremlin-1/Drm is crucial in embryo-/organogenesis and has been shown to be expressed in the adult organism at sites of arterial injury and to inhibit monocyte migration. The purpose of the present study was to evaluate and characterize the role of Gremlin-1 in atherosclerosis. Here we report that Gremlin-1 is highly expressed primarily by monocytes/macrophages in aortic atherosclerotic lesions of ApoE -/- mice and is secreted from activated monocytes and during macrophage development in vitro. Gremlin-1 reduces macrophage formation by inhibiting macrophage migration inhibitory factor (MIF), a cytokine critically involved in atherosclerotic plaque progression and vulnerability. Gremlin-1 binds with high affinity to MIF (K D = 54 nM), as evidenced by surface plasmon resonance analysis and co-immunoprecipitation, and reduces MIF-induced release of TNF-α from macrophages. Treatment of ApoE -/- mice with a dimeric recombinant fusion protein, mGremlin1-Fc, but not with equimolar control Fc or inactivated mGremlin1-Fc, reduced TNF-α expression, the content of monocytes/macrophages of atherosclerotic lesions, and attenuated atheroprogression. The present data disclose that Gremlin-1 is an endogenous antagonist of MIF and define a role for Gremlin-1/MIF interaction in atherosclerosis.

AB - Monocyte infiltration and macrophage formation are pivotal steps in atherosclerosis and plaque vulnerability. Gremlin-1/Drm is crucial in embryo-/organogenesis and has been shown to be expressed in the adult organism at sites of arterial injury and to inhibit monocyte migration. The purpose of the present study was to evaluate and characterize the role of Gremlin-1 in atherosclerosis. Here we report that Gremlin-1 is highly expressed primarily by monocytes/macrophages in aortic atherosclerotic lesions of ApoE -/- mice and is secreted from activated monocytes and during macrophage development in vitro. Gremlin-1 reduces macrophage formation by inhibiting macrophage migration inhibitory factor (MIF), a cytokine critically involved in atherosclerotic plaque progression and vulnerability. Gremlin-1 binds with high affinity to MIF (K D = 54 nM), as evidenced by surface plasmon resonance analysis and co-immunoprecipitation, and reduces MIF-induced release of TNF-α from macrophages. Treatment of ApoE -/- mice with a dimeric recombinant fusion protein, mGremlin1-Fc, but not with equimolar control Fc or inactivated mGremlin1-Fc, reduced TNF-α expression, the content of monocytes/macrophages of atherosclerotic lesions, and attenuated atheroprogression. The present data disclose that Gremlin-1 is an endogenous antagonist of MIF and define a role for Gremlin-1/MIF interaction in atherosclerosis.

KW - Biology

KW - Atherosclerosis

KW - Chemokines

KW - Inflammation

KW - Monocytes

KW - Vascular biology

KW - Atherosclerosis

KW - Chemokiness

KW - Inflammation

KW - Monocytes

KW - Vascular biology

KW - Sustainability Science

UR - http://www.scopus.com/inward/record.url?scp=84887084756&partnerID=8YFLogxK

UR - https://www.mendeley.com/catalogue/e24240ee-6cda-3e60-b8bd-268a686be667/

U2 - 10.1074/jbc.M113.477745

DO - 10.1074/jbc.M113.477745

M3 - Journal articles

C2 - 24003215

VL - 288

SP - 31635

EP - 31645

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

SN - 0021-9258

IS - 44

ER -

DOI