Cargando…

Evaluation of cancer-derived myocardial impairments using a mouse model

Myocardial damage in cancer patients is emphasized as a cause of death; however, there are not many murine cachexia models to evaluate cancer-derived heart disorder. Using the mouse cachexia model that we established previously, we investigated myocardial damage in tumor-bearing mice. In cachexic mi...

Descripción completa

Detalles Bibliográficos
Autores principales: Miyagawa, Yoshihiro, Nukaga, Shota, Mori, Takuya, Fujiwara-Tani, Rina, Fujii, Kiyomu, Mori, Shiori, Goto, Kei, Kishi, Shingo, Sasaki, Takamitsu, Nakashima, Chie, Ohmori, Hitoshi, Kawahara, Isao, Luo, Yi, Kuniyasu, Hiroki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7566807/
https://www.ncbi.nlm.nih.gov/pubmed/33110478
http://dx.doi.org/10.18632/oncotarget.27759
_version_ 1783596200490958848
author Miyagawa, Yoshihiro
Nukaga, Shota
Mori, Takuya
Fujiwara-Tani, Rina
Fujii, Kiyomu
Mori, Shiori
Goto, Kei
Kishi, Shingo
Sasaki, Takamitsu
Nakashima, Chie
Ohmori, Hitoshi
Kawahara, Isao
Luo, Yi
Kuniyasu, Hiroki
author_facet Miyagawa, Yoshihiro
Nukaga, Shota
Mori, Takuya
Fujiwara-Tani, Rina
Fujii, Kiyomu
Mori, Shiori
Goto, Kei
Kishi, Shingo
Sasaki, Takamitsu
Nakashima, Chie
Ohmori, Hitoshi
Kawahara, Isao
Luo, Yi
Kuniyasu, Hiroki
author_sort Miyagawa, Yoshihiro
collection PubMed
description Myocardial damage in cancer patients is emphasized as a cause of death; however, there are not many murine cachexia models to evaluate cancer-derived heart disorder. Using the mouse cachexia model that we established previously, we investigated myocardial damage in tumor-bearing mice. In cachexic mice, decreased heart weight and myocardial volume, and dilated left ventricular lumen, and atrophied cardiomyocytes were noted. The cardiomyocytes also showed accumulated 8-hydroxydeoxyguanosine, decreased leucine zipper and EF-hand-containing transmembrane protein-1, and increased microtubule-associated protein light chain3-II. Levels of tumor necrosis factor-α and high-mobility group box-1 proteins in the myocardium were increased, and nuclear factor κB, a signaling molecule associated with these proteins, was activated. When rat cardiomyoblasts (H9c2 cells) were treated with mouse cachexia model ascites and subjected to flux analysis, both oxidative phosphorylation and glycolysis were suppressed, and the cells were in a quiescent state. These results are in good agreement with those previously reported on cancerous myocardial damage. The established mouse cachexia model can therefore be considered useful for analyzing cancer-derived myocardial damage.
format Online
Article
Text
id pubmed-7566807
institution National Center for Biotechnology Information
language English
publishDate 2020
publisher Impact Journals LLC
record_format MEDLINE/PubMed
spelling pubmed-75668072020-10-26 Evaluation of cancer-derived myocardial impairments using a mouse model Miyagawa, Yoshihiro Nukaga, Shota Mori, Takuya Fujiwara-Tani, Rina Fujii, Kiyomu Mori, Shiori Goto, Kei Kishi, Shingo Sasaki, Takamitsu Nakashima, Chie Ohmori, Hitoshi Kawahara, Isao Luo, Yi Kuniyasu, Hiroki Oncotarget Research Paper Myocardial damage in cancer patients is emphasized as a cause of death; however, there are not many murine cachexia models to evaluate cancer-derived heart disorder. Using the mouse cachexia model that we established previously, we investigated myocardial damage in tumor-bearing mice. In cachexic mice, decreased heart weight and myocardial volume, and dilated left ventricular lumen, and atrophied cardiomyocytes were noted. The cardiomyocytes also showed accumulated 8-hydroxydeoxyguanosine, decreased leucine zipper and EF-hand-containing transmembrane protein-1, and increased microtubule-associated protein light chain3-II. Levels of tumor necrosis factor-α and high-mobility group box-1 proteins in the myocardium were increased, and nuclear factor κB, a signaling molecule associated with these proteins, was activated. When rat cardiomyoblasts (H9c2 cells) were treated with mouse cachexia model ascites and subjected to flux analysis, both oxidative phosphorylation and glycolysis were suppressed, and the cells were in a quiescent state. These results are in good agreement with those previously reported on cancerous myocardial damage. The established mouse cachexia model can therefore be considered useful for analyzing cancer-derived myocardial damage. Impact Journals LLC 2020-10-13 /pmc/articles/PMC7566807/ /pubmed/33110478 http://dx.doi.org/10.18632/oncotarget.27759 Text en https://creativecommons.org/licenses/by/3.0/ Copyright: © 2020 Miyagawa et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Miyagawa, Yoshihiro
Nukaga, Shota
Mori, Takuya
Fujiwara-Tani, Rina
Fujii, Kiyomu
Mori, Shiori
Goto, Kei
Kishi, Shingo
Sasaki, Takamitsu
Nakashima, Chie
Ohmori, Hitoshi
Kawahara, Isao
Luo, Yi
Kuniyasu, Hiroki
Evaluation of cancer-derived myocardial impairments using a mouse model
title Evaluation of cancer-derived myocardial impairments using a mouse model
title_full Evaluation of cancer-derived myocardial impairments using a mouse model
title_fullStr Evaluation of cancer-derived myocardial impairments using a mouse model
title_full_unstemmed Evaluation of cancer-derived myocardial impairments using a mouse model
title_short Evaluation of cancer-derived myocardial impairments using a mouse model
title_sort evaluation of cancer-derived myocardial impairments using a mouse model
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7566807/
https://www.ncbi.nlm.nih.gov/pubmed/33110478
http://dx.doi.org/10.18632/oncotarget.27759
work_keys_str_mv AT miyagawayoshihiro evaluationofcancerderivedmyocardialimpairmentsusingamousemodel
AT nukagashota evaluationofcancerderivedmyocardialimpairmentsusingamousemodel
AT moritakuya evaluationofcancerderivedmyocardialimpairmentsusingamousemodel
AT fujiwaratanirina evaluationofcancerderivedmyocardialimpairmentsusingamousemodel
AT fujiikiyomu evaluationofcancerderivedmyocardialimpairmentsusingamousemodel
AT morishiori evaluationofcancerderivedmyocardialimpairmentsusingamousemodel
AT gotokei evaluationofcancerderivedmyocardialimpairmentsusingamousemodel
AT kishishingo evaluationofcancerderivedmyocardialimpairmentsusingamousemodel
AT sasakitakamitsu evaluationofcancerderivedmyocardialimpairmentsusingamousemodel
AT nakashimachie evaluationofcancerderivedmyocardialimpairmentsusingamousemodel
AT ohmorihitoshi evaluationofcancerderivedmyocardialimpairmentsusingamousemodel
AT kawaharaisao evaluationofcancerderivedmyocardialimpairmentsusingamousemodel
AT luoyi evaluationofcancerderivedmyocardialimpairmentsusingamousemodel
AT kuniyasuhiroki evaluationofcancerderivedmyocardialimpairmentsusingamousemodel