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Chrono-pharmacological Targeting of the CCL2-CCR2 Axis Ameliorates Atherosclerosis

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Chrono-pharmacological Targeting of the CCL2-CCR2 Axis Ameliorates Atherosclerosis. / Winter, Carla; Silvestre-Roig, Carlos; Ortega-Gomez, Almudena; Lemnitzer, Patricia; Poelman, Hessel; Schumski, Ariane; Winter, Janine; Drechsler, Maik; de Jong, Renske; Immler, Roland; Sperandio, Markus; Hristov, Michael; Zeller, Tanja; Nicolaes, Gerry A F; Weber, Christian; Viola, Joana R; Hidalgo, Andres; Scheiermann, Christoph; Soehnlein, Oliver.

in: CELL METAB, Jahrgang 28, Nr. 1, 03.07.2018, S. 175-182.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Winter, C, Silvestre-Roig, C, Ortega-Gomez, A, Lemnitzer, P, Poelman, H, Schumski, A, Winter, J, Drechsler, M, de Jong, R, Immler, R, Sperandio, M, Hristov, M, Zeller, T, Nicolaes, GAF, Weber, C, Viola, JR, Hidalgo, A, Scheiermann, C & Soehnlein, O 2018, 'Chrono-pharmacological Targeting of the CCL2-CCR2 Axis Ameliorates Atherosclerosis', CELL METAB, Jg. 28, Nr. 1, S. 175-182. https://doi.org/10.1016/j.cmet.2018.05.002

APA

Winter, C., Silvestre-Roig, C., Ortega-Gomez, A., Lemnitzer, P., Poelman, H., Schumski, A., Winter, J., Drechsler, M., de Jong, R., Immler, R., Sperandio, M., Hristov, M., Zeller, T., Nicolaes, G. A. F., Weber, C., Viola, J. R., Hidalgo, A., Scheiermann, C., & Soehnlein, O. (2018). Chrono-pharmacological Targeting of the CCL2-CCR2 Axis Ameliorates Atherosclerosis. CELL METAB, 28(1), 175-182. https://doi.org/10.1016/j.cmet.2018.05.002

Vancouver

Winter C, Silvestre-Roig C, Ortega-Gomez A, Lemnitzer P, Poelman H, Schumski A et al. Chrono-pharmacological Targeting of the CCL2-CCR2 Axis Ameliorates Atherosclerosis. CELL METAB. 2018 Jul 3;28(1):175-182. https://doi.org/10.1016/j.cmet.2018.05.002

Bibtex

@article{40084fd3546f4b4b9fe553a8c095e95d,
title = "Chrono-pharmacological Targeting of the CCL2-CCR2 Axis Ameliorates Atherosclerosis",
abstract = "Onset of cardiovascular complications as a consequence of atherosclerosis exhibits a circadian incidence with a peak in the morning hours. Although development of atherosclerosis extends for long periods of time through arterial leukocyte recruitment, we hypothesized that discrete diurnal invasion of the arterial wall could sustain atherogenic growth. Here, we show that myeloid cell recruitment to atherosclerotic lesions oscillates with a peak during the transition from the activity to the resting phase. This diurnal phenotype is regulated by rhythmic release of myeloid cell-derived CCL2, and blockade of its signaling abolished oscillatory leukocyte adhesion. In contrast, we show that myeloid cell adhesion to microvascular beds peaks during the early activity phase. Consequently, timed pharmacological CCR2 neutralization during the activity phase caused inhibition of atherosclerosis without disturbing microvascular recruitment. These findings demonstrate that chronic inflammation of large vessels feeds on rhythmic myeloid cell recruitment, and lay the foundation for chrono-pharmacology-based therapy.",
keywords = "Animals, Atherosclerosis/therapy, Cell Adhesion, Chemokine CCL2/metabolism, Inflammation/pathology, Mesenchymal Stem Cells/metabolism, Mice, Mice, Inbred C57BL, Mice, Knockout, Myeloid Cells/metabolism, Receptors, CCR2/metabolism, Signal Transduction",
author = "Carla Winter and Carlos Silvestre-Roig and Almudena Ortega-Gomez and Patricia Lemnitzer and Hessel Poelman and Ariane Schumski and Janine Winter and Maik Drechsler and {de Jong}, Renske and Roland Immler and Markus Sperandio and Michael Hristov and Tanja Zeller and Nicolaes, {Gerry A F} and Christian Weber and Viola, {Joana R} and Andres Hidalgo and Christoph Scheiermann and Oliver Soehnlein",
note = "Copyright {\textcopyright} 2018 Elsevier Inc. All rights reserved.",
year = "2018",
month = jul,
day = "3",
doi = "10.1016/j.cmet.2018.05.002",
language = "English",
volume = "28",
pages = "175--182",
journal = "CELL METAB",
issn = "1550-4131",
publisher = "Cell Press",
number = "1",

}

RIS

TY - JOUR

T1 - Chrono-pharmacological Targeting of the CCL2-CCR2 Axis Ameliorates Atherosclerosis

AU - Winter, Carla

AU - Silvestre-Roig, Carlos

AU - Ortega-Gomez, Almudena

AU - Lemnitzer, Patricia

AU - Poelman, Hessel

AU - Schumski, Ariane

AU - Winter, Janine

AU - Drechsler, Maik

AU - de Jong, Renske

AU - Immler, Roland

AU - Sperandio, Markus

AU - Hristov, Michael

AU - Zeller, Tanja

AU - Nicolaes, Gerry A F

AU - Weber, Christian

AU - Viola, Joana R

AU - Hidalgo, Andres

AU - Scheiermann, Christoph

AU - Soehnlein, Oliver

N1 - Copyright © 2018 Elsevier Inc. All rights reserved.

PY - 2018/7/3

Y1 - 2018/7/3

N2 - Onset of cardiovascular complications as a consequence of atherosclerosis exhibits a circadian incidence with a peak in the morning hours. Although development of atherosclerosis extends for long periods of time through arterial leukocyte recruitment, we hypothesized that discrete diurnal invasion of the arterial wall could sustain atherogenic growth. Here, we show that myeloid cell recruitment to atherosclerotic lesions oscillates with a peak during the transition from the activity to the resting phase. This diurnal phenotype is regulated by rhythmic release of myeloid cell-derived CCL2, and blockade of its signaling abolished oscillatory leukocyte adhesion. In contrast, we show that myeloid cell adhesion to microvascular beds peaks during the early activity phase. Consequently, timed pharmacological CCR2 neutralization during the activity phase caused inhibition of atherosclerosis without disturbing microvascular recruitment. These findings demonstrate that chronic inflammation of large vessels feeds on rhythmic myeloid cell recruitment, and lay the foundation for chrono-pharmacology-based therapy.

AB - Onset of cardiovascular complications as a consequence of atherosclerosis exhibits a circadian incidence with a peak in the morning hours. Although development of atherosclerosis extends for long periods of time through arterial leukocyte recruitment, we hypothesized that discrete diurnal invasion of the arterial wall could sustain atherogenic growth. Here, we show that myeloid cell recruitment to atherosclerotic lesions oscillates with a peak during the transition from the activity to the resting phase. This diurnal phenotype is regulated by rhythmic release of myeloid cell-derived CCL2, and blockade of its signaling abolished oscillatory leukocyte adhesion. In contrast, we show that myeloid cell adhesion to microvascular beds peaks during the early activity phase. Consequently, timed pharmacological CCR2 neutralization during the activity phase caused inhibition of atherosclerosis without disturbing microvascular recruitment. These findings demonstrate that chronic inflammation of large vessels feeds on rhythmic myeloid cell recruitment, and lay the foundation for chrono-pharmacology-based therapy.

KW - Animals

KW - Atherosclerosis/therapy

KW - Cell Adhesion

KW - Chemokine CCL2/metabolism

KW - Inflammation/pathology

KW - Mesenchymal Stem Cells/metabolism

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Myeloid Cells/metabolism

KW - Receptors, CCR2/metabolism

KW - Signal Transduction

U2 - 10.1016/j.cmet.2018.05.002

DO - 10.1016/j.cmet.2018.05.002

M3 - SCORING: Journal article

C2 - 29861387

VL - 28

SP - 175

EP - 182

JO - CELL METAB

JF - CELL METAB

SN - 1550-4131

IS - 1

ER -