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Ly6C(low) and Not Ly6C(high) Macrophages Accumulate First in the Heart in a Model of Murine Pressure-Overload
Cardiac tissue remodeling in the course of chronic left ventricular hypertrophy requires phagocytes which degrade cellular debris, initiate and maintain tissue inflammation and reorganization. The dynamics of phagocytes in left ventricular hypertrophy have not been systematically studied. Here, we c...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4240580/ https://www.ncbi.nlm.nih.gov/pubmed/25415601 http://dx.doi.org/10.1371/journal.pone.0112710 |
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author | Weisheit, Christina Zhang, Yunyang Faron, Anton Köpke, Odilia Weisheit, Gunnar Steinsträsser, Arne Frede, Stilla Meyer, Rainer Boehm, Olaf Hoeft, Andreas Kurts, Christian Baumgarten, Georg |
author_facet | Weisheit, Christina Zhang, Yunyang Faron, Anton Köpke, Odilia Weisheit, Gunnar Steinsträsser, Arne Frede, Stilla Meyer, Rainer Boehm, Olaf Hoeft, Andreas Kurts, Christian Baumgarten, Georg |
author_sort | Weisheit, Christina |
collection | PubMed |
description | Cardiac tissue remodeling in the course of chronic left ventricular hypertrophy requires phagocytes which degrade cellular debris, initiate and maintain tissue inflammation and reorganization. The dynamics of phagocytes in left ventricular hypertrophy have not been systematically studied. Here, we characterized the temporal accumulation of leukocytes in the cardiac immune response by flow cytometry and fluorescence microscopy at day 3, 6 and 21 following transverse aortic constriction (TAC). Cardiac hypertrophy due to chronic pressure overload causes cardiac immune response and inflammation represented by an increase of immune cells at all three time points among which neutrophils reached their maximum at day 3 and macrophages at day 6. The cardiac macrophage population consisted of both Ly6C(low) and Ly6C(high) macrophages. Ly6C(low) macrophages were more abundant peaking at day 6 in response to pressure overload. During the development of cardiac hypertrophy the expression pattern of adhesion molecules was investigated by qRT-PCR and flow cytometry. CD11b, CX3CR1 and ICAM-1 determined by qRT-PCR in whole cardiac tissue were up-regulated in response to pressure overload at day 3 and 6. CD11b and CX3CR1 were significantly increased by TAC on the surface of Ly6C(low) but not on Ly6C(high) macrophages. Furthermore, ICAM-1 was up-regulated on cardiac endothelial cells. In fluorescence microscopy Ly6C(low) macrophages could be observed attached to the intra- and extra-vascular vessel-wall. Taken together, TAC induced the expression of adhesion molecules, which may explain the accumulation of Ly6C(low) macrophages in the cardiac tissue, where these cells might contribute to cardiac inflammation and remodeling in response to pressure overload. |
format | Online Article Text |
id | pubmed-4240580 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-42405802014-11-26 Ly6C(low) and Not Ly6C(high) Macrophages Accumulate First in the Heart in a Model of Murine Pressure-Overload Weisheit, Christina Zhang, Yunyang Faron, Anton Köpke, Odilia Weisheit, Gunnar Steinsträsser, Arne Frede, Stilla Meyer, Rainer Boehm, Olaf Hoeft, Andreas Kurts, Christian Baumgarten, Georg PLoS One Research Article Cardiac tissue remodeling in the course of chronic left ventricular hypertrophy requires phagocytes which degrade cellular debris, initiate and maintain tissue inflammation and reorganization. The dynamics of phagocytes in left ventricular hypertrophy have not been systematically studied. Here, we characterized the temporal accumulation of leukocytes in the cardiac immune response by flow cytometry and fluorescence microscopy at day 3, 6 and 21 following transverse aortic constriction (TAC). Cardiac hypertrophy due to chronic pressure overload causes cardiac immune response and inflammation represented by an increase of immune cells at all three time points among which neutrophils reached their maximum at day 3 and macrophages at day 6. The cardiac macrophage population consisted of both Ly6C(low) and Ly6C(high) macrophages. Ly6C(low) macrophages were more abundant peaking at day 6 in response to pressure overload. During the development of cardiac hypertrophy the expression pattern of adhesion molecules was investigated by qRT-PCR and flow cytometry. CD11b, CX3CR1 and ICAM-1 determined by qRT-PCR in whole cardiac tissue were up-regulated in response to pressure overload at day 3 and 6. CD11b and CX3CR1 were significantly increased by TAC on the surface of Ly6C(low) but not on Ly6C(high) macrophages. Furthermore, ICAM-1 was up-regulated on cardiac endothelial cells. In fluorescence microscopy Ly6C(low) macrophages could be observed attached to the intra- and extra-vascular vessel-wall. Taken together, TAC induced the expression of adhesion molecules, which may explain the accumulation of Ly6C(low) macrophages in the cardiac tissue, where these cells might contribute to cardiac inflammation and remodeling in response to pressure overload. Public Library of Science 2014-11-21 /pmc/articles/PMC4240580/ /pubmed/25415601 http://dx.doi.org/10.1371/journal.pone.0112710 Text en © 2014 Weisheit et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Weisheit, Christina Zhang, Yunyang Faron, Anton Köpke, Odilia Weisheit, Gunnar Steinsträsser, Arne Frede, Stilla Meyer, Rainer Boehm, Olaf Hoeft, Andreas Kurts, Christian Baumgarten, Georg Ly6C(low) and Not Ly6C(high) Macrophages Accumulate First in the Heart in a Model of Murine Pressure-Overload |
title | Ly6C(low) and Not Ly6C(high) Macrophages Accumulate First in the Heart in a Model of Murine Pressure-Overload |
title_full | Ly6C(low) and Not Ly6C(high) Macrophages Accumulate First in the Heart in a Model of Murine Pressure-Overload |
title_fullStr | Ly6C(low) and Not Ly6C(high) Macrophages Accumulate First in the Heart in a Model of Murine Pressure-Overload |
title_full_unstemmed | Ly6C(low) and Not Ly6C(high) Macrophages Accumulate First in the Heart in a Model of Murine Pressure-Overload |
title_short | Ly6C(low) and Not Ly6C(high) Macrophages Accumulate First in the Heart in a Model of Murine Pressure-Overload |
title_sort | ly6c(low) and not ly6c(high) macrophages accumulate first in the heart in a model of murine pressure-overload |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4240580/ https://www.ncbi.nlm.nih.gov/pubmed/25415601 http://dx.doi.org/10.1371/journal.pone.0112710 |
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