Three TF Co-expression Modules Regulate Pressure-Overload Cardiac Hypertrophy in Male Mice

Abstract Pathological cardiac hypertrophy, a dynamic remodeling process, is a major risk factor for heart failure. Although a number of key regulators and related genes have been identified, how the transcription factors (TFs) dynamically regulate the associated genes and control the morphological a...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Yao-Ming Chang, Li Ling, Ya-Ting Chang, Yu-Wang Chang, Wen-Hsiung Li, Arthur Chun-Chieh Shih, Chien-Chang Chen
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/e6c3c3b0dd254a86b4559886f5ceded0
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:e6c3c3b0dd254a86b4559886f5ceded0
record_format	dspace
spelling	oai:doaj.org-article:e6c3c3b0dd254a86b4559886f5ceded02021-12-02T12:30:45ZThree TF Co-expression Modules Regulate Pressure-Overload Cardiac Hypertrophy in Male Mice10.1038/s41598-017-07981-42045-2322https://doaj.org/article/e6c3c3b0dd254a86b4559886f5ceded02017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-07981-4https://doaj.org/toc/2045-2322Abstract Pathological cardiac hypertrophy, a dynamic remodeling process, is a major risk factor for heart failure. Although a number of key regulators and related genes have been identified, how the transcription factors (TFs) dynamically regulate the associated genes and control the morphological and electrophysiological changes during the hypertrophic process are still largely unknown. In this study, we obtained the time-course transcriptomes at five time points in four weeks from male murine hearts subjected to transverse aorta banding surgery. From a series of computational analyses, we identified three major co-expression modules of TF genes that may regulate the gene expression changes during the development of cardiac hypertrophy in mice. After pressure overload, the TF genes in Module 1 were up-regulated before the occurrence of significant morphological changes and one week later were down-regulated gradually, while those in Modules 2 and 3 took over the regulation as the heart size increased. Our analyses revealed that the TF genes up-regulated at the early stages likely initiated the cascading regulation and most of the well-known cardiac miRNAs were up-regulated at later stages for suppression. In addition, the constructed time-dependent regulatory network reveals some TFs including Egr2 as new candidate key regulators of cardiovascular-associated (CV) genes.Yao-Ming ChangLi LingYa-Ting ChangYu-Wang ChangWen-Hsiung LiArthur Chun-Chieh ShihChien-Chang ChenNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Yao-Ming Chang Li Ling Ya-Ting Chang Yu-Wang Chang Wen-Hsiung Li Arthur Chun-Chieh Shih Chien-Chang Chen Three TF Co-expression Modules Regulate Pressure-Overload Cardiac Hypertrophy in Male Mice
description	Abstract Pathological cardiac hypertrophy, a dynamic remodeling process, is a major risk factor for heart failure. Although a number of key regulators and related genes have been identified, how the transcription factors (TFs) dynamically regulate the associated genes and control the morphological and electrophysiological changes during the hypertrophic process are still largely unknown. In this study, we obtained the time-course transcriptomes at five time points in four weeks from male murine hearts subjected to transverse aorta banding surgery. From a series of computational analyses, we identified three major co-expression modules of TF genes that may regulate the gene expression changes during the development of cardiac hypertrophy in mice. After pressure overload, the TF genes in Module 1 were up-regulated before the occurrence of significant morphological changes and one week later were down-regulated gradually, while those in Modules 2 and 3 took over the regulation as the heart size increased. Our analyses revealed that the TF genes up-regulated at the early stages likely initiated the cascading regulation and most of the well-known cardiac miRNAs were up-regulated at later stages for suppression. In addition, the constructed time-dependent regulatory network reveals some TFs including Egr2 as new candidate key regulators of cardiovascular-associated (CV) genes.
format	article
author	Yao-Ming Chang Li Ling Ya-Ting Chang Yu-Wang Chang Wen-Hsiung Li Arthur Chun-Chieh Shih Chien-Chang Chen
author_facet	Yao-Ming Chang Li Ling Ya-Ting Chang Yu-Wang Chang Wen-Hsiung Li Arthur Chun-Chieh Shih Chien-Chang Chen
author_sort	Yao-Ming Chang
title	Three TF Co-expression Modules Regulate Pressure-Overload Cardiac Hypertrophy in Male Mice
title_short	Three TF Co-expression Modules Regulate Pressure-Overload Cardiac Hypertrophy in Male Mice
title_full	Three TF Co-expression Modules Regulate Pressure-Overload Cardiac Hypertrophy in Male Mice
title_fullStr	Three TF Co-expression Modules Regulate Pressure-Overload Cardiac Hypertrophy in Male Mice
title_full_unstemmed	Three TF Co-expression Modules Regulate Pressure-Overload Cardiac Hypertrophy in Male Mice
title_sort	three tf co-expression modules regulate pressure-overload cardiac hypertrophy in male mice
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/e6c3c3b0dd254a86b4559886f5ceded0
work_keys_str_mv	AT yaomingchang threetfcoexpressionmodulesregulatepressureoverloadcardiachypertrophyinmalemice AT liling threetfcoexpressionmodulesregulatepressureoverloadcardiachypertrophyinmalemice AT yatingchang threetfcoexpressionmodulesregulatepressureoverloadcardiachypertrophyinmalemice AT yuwangchang threetfcoexpressionmodulesregulatepressureoverloadcardiachypertrophyinmalemice AT wenhsiungli threetfcoexpressionmodulesregulatepressureoverloadcardiachypertrophyinmalemice AT arthurchunchiehshih threetfcoexpressionmodulesregulatepressureoverloadcardiachypertrophyinmalemice AT chienchangchen threetfcoexpressionmodulesregulatepressureoverloadcardiachypertrophyinmalemice
_version_	1718394369172570112

Three TF Co-expression Modules Regulate Pressure-Overload Cardiac Hypertrophy in Male Mice

Ejemplares similares