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Pressure Overload-induced Cardiac Remodeling and Dysfunction in the Absence of Interleukin 6 in Mice
Congestive heart failure is associated with increased expression of pro-inflammatory cytokines, and the levels of these cytokines correlate with heart failure severity and prognosis. Chronic interleukin 6 (IL-6) stimulation leads to LV hypertrophy and dysfunction, and deletion of IL-6 reduces LV hyp...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3482286/ https://www.ncbi.nlm.nih.gov/pubmed/22825686 http://dx.doi.org/10.1038/labinvest.2012.97 |
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author | Lai, N. Chin Gao, Mei Hua Tang, Eric Tang, Ruoying Guo, Tracy Dalton, Nancy D. Deng, Aihua Tang, Tong |
author_facet | Lai, N. Chin Gao, Mei Hua Tang, Eric Tang, Ruoying Guo, Tracy Dalton, Nancy D. Deng, Aihua Tang, Tong |
author_sort | Lai, N. Chin |
collection | PubMed |
description | Congestive heart failure is associated with increased expression of pro-inflammatory cytokines, and the levels of these cytokines correlate with heart failure severity and prognosis. Chronic interleukin 6 (IL-6) stimulation leads to LV hypertrophy and dysfunction, and deletion of IL-6 reduces LV hypertrophy after angiotensin II infusion. In this study, we tested the hypothesis that IL-6 deletion has favorable effects on pressure-overloaded hearts. We performed transverse aortic constriction on IL-6-deleted (IL6KO) mice and C57BL/6J mice (CON) to induce pressure overload. Pressure overload was associated with similar LV hypertrophy, dilation, and dysfunction in CON and IL6KO mice. Re-activation of the fetal gene program was also similar in pressure-overloaded CON and IL6KO mice. There were no differences between CON and IL6KO mice in LV fibrosis or expression of extracellular matrix proteins after pressure overload. In addition, no group differences in apoptosis or autophagy were seen. These data indicate that IL-6 deletion does not block LV remodeling and dysfunction induced by pressure overload. Attenuated content of interleukin 11 appears to be a compensatory mechanism for IL-6 deletion in pressure-overloaded hearts. We infer from these data that limiting availability of IL-6 alone is not sufficient to attenuate LV remodeling and dysfunction in failing hearts. |
format | Online Article Text |
id | pubmed-3482286 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
record_format | MEDLINE/PubMed |
spelling | pubmed-34822862013-05-01 Pressure Overload-induced Cardiac Remodeling and Dysfunction in the Absence of Interleukin 6 in Mice Lai, N. Chin Gao, Mei Hua Tang, Eric Tang, Ruoying Guo, Tracy Dalton, Nancy D. Deng, Aihua Tang, Tong Lab Invest Article Congestive heart failure is associated with increased expression of pro-inflammatory cytokines, and the levels of these cytokines correlate with heart failure severity and prognosis. Chronic interleukin 6 (IL-6) stimulation leads to LV hypertrophy and dysfunction, and deletion of IL-6 reduces LV hypertrophy after angiotensin II infusion. In this study, we tested the hypothesis that IL-6 deletion has favorable effects on pressure-overloaded hearts. We performed transverse aortic constriction on IL-6-deleted (IL6KO) mice and C57BL/6J mice (CON) to induce pressure overload. Pressure overload was associated with similar LV hypertrophy, dilation, and dysfunction in CON and IL6KO mice. Re-activation of the fetal gene program was also similar in pressure-overloaded CON and IL6KO mice. There were no differences between CON and IL6KO mice in LV fibrosis or expression of extracellular matrix proteins after pressure overload. In addition, no group differences in apoptosis or autophagy were seen. These data indicate that IL-6 deletion does not block LV remodeling and dysfunction induced by pressure overload. Attenuated content of interleukin 11 appears to be a compensatory mechanism for IL-6 deletion in pressure-overloaded hearts. We infer from these data that limiting availability of IL-6 alone is not sufficient to attenuate LV remodeling and dysfunction in failing hearts. 2012-07-23 2012-11 /pmc/articles/PMC3482286/ /pubmed/22825686 http://dx.doi.org/10.1038/labinvest.2012.97 Text en Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms |
spellingShingle | Article Lai, N. Chin Gao, Mei Hua Tang, Eric Tang, Ruoying Guo, Tracy Dalton, Nancy D. Deng, Aihua Tang, Tong Pressure Overload-induced Cardiac Remodeling and Dysfunction in the Absence of Interleukin 6 in Mice |
title | Pressure Overload-induced Cardiac Remodeling and Dysfunction in the Absence of Interleukin 6 in Mice |
title_full | Pressure Overload-induced Cardiac Remodeling and Dysfunction in the Absence of Interleukin 6 in Mice |
title_fullStr | Pressure Overload-induced Cardiac Remodeling and Dysfunction in the Absence of Interleukin 6 in Mice |
title_full_unstemmed | Pressure Overload-induced Cardiac Remodeling and Dysfunction in the Absence of Interleukin 6 in Mice |
title_short | Pressure Overload-induced Cardiac Remodeling and Dysfunction in the Absence of Interleukin 6 in Mice |
title_sort | pressure overload-induced cardiac remodeling and dysfunction in the absence of interleukin 6 in mice |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3482286/ https://www.ncbi.nlm.nih.gov/pubmed/22825686 http://dx.doi.org/10.1038/labinvest.2012.97 |
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