Cancer induces cardiomyocyte remodeling and hypoinnervation in the left ventricle of the mouse heart.
Cancer is often associated with cachexia, cardiovascular symptoms and autonomic dysregulation. We tested whether extracardiac cancer directly affects the innervation of left ventricular myocardium. Mice injected with Lewis lung carcinoma cells (tumor group, TG) or PBS (control group, CG) were analyz...
Guardado en:
Autores principales: | , , , , , , , , |
---|---|
Formato: | article |
Lenguaje: | EN |
Publicado: |
Public Library of Science (PLoS)
2011
|
Materias: | |
Acceso en línea: | https://doaj.org/article/f9d2dd92aea9406e8427fa1f3dd5d3c9 |
Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
id |
oai:doaj.org-article:f9d2dd92aea9406e8427fa1f3dd5d3c9 |
---|---|
record_format |
dspace |
spelling |
oai:doaj.org-article:f9d2dd92aea9406e8427fa1f3dd5d3c92021-11-18T06:53:10ZCancer induces cardiomyocyte remodeling and hypoinnervation in the left ventricle of the mouse heart.1932-620310.1371/journal.pone.0020424https://doaj.org/article/f9d2dd92aea9406e8427fa1f3dd5d3c92011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21637823/?tool=EBIhttps://doaj.org/toc/1932-6203Cancer is often associated with cachexia, cardiovascular symptoms and autonomic dysregulation. We tested whether extracardiac cancer directly affects the innervation of left ventricular myocardium. Mice injected with Lewis lung carcinoma cells (tumor group, TG) or PBS (control group, CG) were analyzed after 21 days. Cardiac function (echocardiography), serum levels of TNF-α and Il-6 (ELISA), structural alterations of cardiomyocytes and their innervation (design-based stereology) and levels of innervation-related mRNA (quantitative RT-PCR) were analysed. The groups did not differ in various functional parameters. Serum levels of TNF-α and Il-6 were elevated in TG. The total length of axons in the left ventricle was reduced. The number of dense core vesicles per axon profile was reduced. Decreased myofibrillar volume, increased sarcoplasmic volume and increased volume of lipid droplets were indicative of metabolic alterations of TG cardiomyocytes. In the heart, the mRNA level of nerve growth factor was reduced whereas that of β1-adrenergic receptor was unchanged in TG. In the stellate ganglion of TG, mRNA levels of nerve growth factor and neuropeptide Y were decreased and that of tyrosine hydroxylase was increased. In summary, cancer induces a systemic pro-inflammatory state, a significant reduction in myocardial innervation and a catabolic phenotype of cardiomyocytes in the mouse. Reduced expression of nerve growth factor may account for the reduced myocardial innervation.Christian MühlfeldSuman Kumar DasFrank R HeinzelAlbrecht SchmidtHeiner PostSilvia SchauerTamara PapadakisWolfgang KummerGerald HoeflerPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 5, p e20424 (2011) |
institution |
DOAJ |
collection |
DOAJ |
language |
EN |
topic |
Medicine R Science Q |
spellingShingle |
Medicine R Science Q Christian Mühlfeld Suman Kumar Das Frank R Heinzel Albrecht Schmidt Heiner Post Silvia Schauer Tamara Papadakis Wolfgang Kummer Gerald Hoefler Cancer induces cardiomyocyte remodeling and hypoinnervation in the left ventricle of the mouse heart. |
description |
Cancer is often associated with cachexia, cardiovascular symptoms and autonomic dysregulation. We tested whether extracardiac cancer directly affects the innervation of left ventricular myocardium. Mice injected with Lewis lung carcinoma cells (tumor group, TG) or PBS (control group, CG) were analyzed after 21 days. Cardiac function (echocardiography), serum levels of TNF-α and Il-6 (ELISA), structural alterations of cardiomyocytes and their innervation (design-based stereology) and levels of innervation-related mRNA (quantitative RT-PCR) were analysed. The groups did not differ in various functional parameters. Serum levels of TNF-α and Il-6 were elevated in TG. The total length of axons in the left ventricle was reduced. The number of dense core vesicles per axon profile was reduced. Decreased myofibrillar volume, increased sarcoplasmic volume and increased volume of lipid droplets were indicative of metabolic alterations of TG cardiomyocytes. In the heart, the mRNA level of nerve growth factor was reduced whereas that of β1-adrenergic receptor was unchanged in TG. In the stellate ganglion of TG, mRNA levels of nerve growth factor and neuropeptide Y were decreased and that of tyrosine hydroxylase was increased. In summary, cancer induces a systemic pro-inflammatory state, a significant reduction in myocardial innervation and a catabolic phenotype of cardiomyocytes in the mouse. Reduced expression of nerve growth factor may account for the reduced myocardial innervation. |
format |
article |
author |
Christian Mühlfeld Suman Kumar Das Frank R Heinzel Albrecht Schmidt Heiner Post Silvia Schauer Tamara Papadakis Wolfgang Kummer Gerald Hoefler |
author_facet |
Christian Mühlfeld Suman Kumar Das Frank R Heinzel Albrecht Schmidt Heiner Post Silvia Schauer Tamara Papadakis Wolfgang Kummer Gerald Hoefler |
author_sort |
Christian Mühlfeld |
title |
Cancer induces cardiomyocyte remodeling and hypoinnervation in the left ventricle of the mouse heart. |
title_short |
Cancer induces cardiomyocyte remodeling and hypoinnervation in the left ventricle of the mouse heart. |
title_full |
Cancer induces cardiomyocyte remodeling and hypoinnervation in the left ventricle of the mouse heart. |
title_fullStr |
Cancer induces cardiomyocyte remodeling and hypoinnervation in the left ventricle of the mouse heart. |
title_full_unstemmed |
Cancer induces cardiomyocyte remodeling and hypoinnervation in the left ventricle of the mouse heart. |
title_sort |
cancer induces cardiomyocyte remodeling and hypoinnervation in the left ventricle of the mouse heart. |
publisher |
Public Library of Science (PLoS) |
publishDate |
2011 |
url |
https://doaj.org/article/f9d2dd92aea9406e8427fa1f3dd5d3c9 |
work_keys_str_mv |
AT christianmuhlfeld cancerinducescardiomyocyteremodelingandhypoinnervationintheleftventricleofthemouseheart AT sumankumardas cancerinducescardiomyocyteremodelingandhypoinnervationintheleftventricleofthemouseheart AT frankrheinzel cancerinducescardiomyocyteremodelingandhypoinnervationintheleftventricleofthemouseheart AT albrechtschmidt cancerinducescardiomyocyteremodelingandhypoinnervationintheleftventricleofthemouseheart AT heinerpost cancerinducescardiomyocyteremodelingandhypoinnervationintheleftventricleofthemouseheart AT silviaschauer cancerinducescardiomyocyteremodelingandhypoinnervationintheleftventricleofthemouseheart AT tamarapapadakis cancerinducescardiomyocyteremodelingandhypoinnervationintheleftventricleofthemouseheart AT wolfgangkummer cancerinducescardiomyocyteremodelingandhypoinnervationintheleftventricleofthemouseheart AT geraldhoefler cancerinducescardiomyocyteremodelingandhypoinnervationintheleftventricleofthemouseheart |
_version_ |
1718424267769511936 |