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Gata6+ Pericardial Cavity Macrophages Relocate to the Injured Heart and Prevent Cardiac Fibrosis

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Gata6+ Pericardial Cavity Macrophages Relocate to the Injured Heart and Prevent Cardiac Fibrosis. / Deniset, Justin F; Belke, Darrell; Lee, Woo-Yong; Jorch, Selina K; Deppermann, Carsten; Hassanabad, Ali Fatehi; Turnbull, Jeannine D; Teng, Guoqi; Rozich, Isaiah; Hudspeth, Kelly; Kanno, Yuka; Brooks, Stephen R; Hadjantonakis, Anna-Katerina; O'Shea, John J; Weber, Georg F; Fedak, Paul W M; Kubes, Paul.

In: IMMUNITY, Vol. 51, No. 1, 16.07.2019, p. 131-140.e5.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Deniset, JF, Belke, D, Lee, W-Y, Jorch, SK, Deppermann, C, Hassanabad, AF, Turnbull, JD, Teng, G, Rozich, I, Hudspeth, K, Kanno, Y, Brooks, SR, Hadjantonakis, A-K, O'Shea, JJ, Weber, GF, Fedak, PWM & Kubes, P 2019, 'Gata6+ Pericardial Cavity Macrophages Relocate to the Injured Heart and Prevent Cardiac Fibrosis', IMMUNITY, vol. 51, no. 1, pp. 131-140.e5. https://doi.org/10.1016/j.immuni.2019.06.010

APA

Deniset, J. F., Belke, D., Lee, W-Y., Jorch, S. K., Deppermann, C., Hassanabad, A. F., Turnbull, J. D., Teng, G., Rozich, I., Hudspeth, K., Kanno, Y., Brooks, S. R., Hadjantonakis, A-K., O'Shea, J. J., Weber, G. F., Fedak, P. W. M., & Kubes, P. (2019). Gata6+ Pericardial Cavity Macrophages Relocate to the Injured Heart and Prevent Cardiac Fibrosis. IMMUNITY, 51(1), 131-140.e5. https://doi.org/10.1016/j.immuni.2019.06.010

Vancouver

Deniset JF, Belke D, Lee W-Y, Jorch SK, Deppermann C, Hassanabad AF et al. Gata6+ Pericardial Cavity Macrophages Relocate to the Injured Heart and Prevent Cardiac Fibrosis. IMMUNITY. 2019 Jul 16;51(1):131-140.e5. https://doi.org/10.1016/j.immuni.2019.06.010

Bibtex

@article{c0e72e48ce4f424880fd3e1b517c410d,
title = "Gata6+ Pericardial Cavity Macrophages Relocate to the Injured Heart and Prevent Cardiac Fibrosis",
abstract = "Macrophages play an important role in structural cardiac remodeling and the transition to heart failure following myocardial infarction (MI). Previous research has focused on the impact of blood-derived monocytes on cardiac repair. Here we examined the contribution of resident cavity macrophages located in the pericardial space adjacent to the site of injury. We found that disruption of the pericardial cavity accelerated maladaptive post-MI cardiac remodeling. Gata6+ macrophages in mouse pericardial fluid contributed to the reparative immune response. Following experimental MI, these macrophages invaded the epicardium and lost Gata6 expression but continued to perform anti-fibrotic functions. Loss of this specialized macrophage population enhanced interstitial fibrosis after ischemic injury. Gata6+ macrophages were present in human pericardial fluid, supporting the notion that this reparative function is relevant in human disease. Our findings uncover an immune cardioprotective role for the pericardial tissue compartment and argue for the reevaluation of surgical procedures that remove the pericardium.",
keywords = "Animals, Cell Movement, Cells, Cultured, Fibrosis/prevention & control, GATA6 Transcription Factor/metabolism, Heart/physiology, Humans, Macrophages/immunology, Mice, Mice, Inbred C57BL, Mice, Transgenic, Myocardial Infarction/immunology, Myocardium/pathology, Pericardium/immunology, Ventricular Remodeling",
author = "Deniset, {Justin F} and Darrell Belke and Woo-Yong Lee and Jorch, {Selina K} and Carsten Deppermann and Hassanabad, {Ali Fatehi} and Turnbull, {Jeannine D} and Guoqi Teng and Isaiah Rozich and Kelly Hudspeth and Yuka Kanno and Brooks, {Stephen R} and Anna-Katerina Hadjantonakis and O'Shea, {John J} and Weber, {Georg F} and Fedak, {Paul W M} and Paul Kubes",
note = "Copyright {\textcopyright} 2019 Elsevier Inc. All rights reserved.",
year = "2019",
month = jul,
day = "16",
doi = "10.1016/j.immuni.2019.06.010",
language = "English",
volume = "51",
pages = "131--140.e5",
journal = "IMMUNITY",
issn = "1074-7613",
publisher = "Cell Press",
number = "1",

}

RIS

TY - JOUR

T1 - Gata6+ Pericardial Cavity Macrophages Relocate to the Injured Heart and Prevent Cardiac Fibrosis

AU - Deniset, Justin F

AU - Belke, Darrell

AU - Lee, Woo-Yong

AU - Jorch, Selina K

AU - Deppermann, Carsten

AU - Hassanabad, Ali Fatehi

AU - Turnbull, Jeannine D

AU - Teng, Guoqi

AU - Rozich, Isaiah

AU - Hudspeth, Kelly

AU - Kanno, Yuka

AU - Brooks, Stephen R

AU - Hadjantonakis, Anna-Katerina

AU - O'Shea, John J

AU - Weber, Georg F

AU - Fedak, Paul W M

AU - Kubes, Paul

N1 - Copyright © 2019 Elsevier Inc. All rights reserved.

PY - 2019/7/16

Y1 - 2019/7/16

N2 - Macrophages play an important role in structural cardiac remodeling and the transition to heart failure following myocardial infarction (MI). Previous research has focused on the impact of blood-derived monocytes on cardiac repair. Here we examined the contribution of resident cavity macrophages located in the pericardial space adjacent to the site of injury. We found that disruption of the pericardial cavity accelerated maladaptive post-MI cardiac remodeling. Gata6+ macrophages in mouse pericardial fluid contributed to the reparative immune response. Following experimental MI, these macrophages invaded the epicardium and lost Gata6 expression but continued to perform anti-fibrotic functions. Loss of this specialized macrophage population enhanced interstitial fibrosis after ischemic injury. Gata6+ macrophages were present in human pericardial fluid, supporting the notion that this reparative function is relevant in human disease. Our findings uncover an immune cardioprotective role for the pericardial tissue compartment and argue for the reevaluation of surgical procedures that remove the pericardium.

AB - Macrophages play an important role in structural cardiac remodeling and the transition to heart failure following myocardial infarction (MI). Previous research has focused on the impact of blood-derived monocytes on cardiac repair. Here we examined the contribution of resident cavity macrophages located in the pericardial space adjacent to the site of injury. We found that disruption of the pericardial cavity accelerated maladaptive post-MI cardiac remodeling. Gata6+ macrophages in mouse pericardial fluid contributed to the reparative immune response. Following experimental MI, these macrophages invaded the epicardium and lost Gata6 expression but continued to perform anti-fibrotic functions. Loss of this specialized macrophage population enhanced interstitial fibrosis after ischemic injury. Gata6+ macrophages were present in human pericardial fluid, supporting the notion that this reparative function is relevant in human disease. Our findings uncover an immune cardioprotective role for the pericardial tissue compartment and argue for the reevaluation of surgical procedures that remove the pericardium.

KW - Animals

KW - Cell Movement

KW - Cells, Cultured

KW - Fibrosis/prevention & control

KW - GATA6 Transcription Factor/metabolism

KW - Heart/physiology

KW - Humans

KW - Macrophages/immunology

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Transgenic

KW - Myocardial Infarction/immunology

KW - Myocardium/pathology

KW - Pericardium/immunology

KW - Ventricular Remodeling

U2 - 10.1016/j.immuni.2019.06.010

DO - 10.1016/j.immuni.2019.06.010

M3 - SCORING: Journal article

C2 - 31315031

VL - 51

SP - 131-140.e5

JO - IMMUNITY

JF - IMMUNITY

SN - 1074-7613

IS - 1

ER -