Enhancement of beta-catenin in cardiomyocytes suppresses survival protein expression but promotes apoptosis and fibrosis

James C. Lin; Wei Wen Kuo; Rathinasamy Baskaran; Ming Cheng Chen; Tsung Jung Ho; Ray Jade Chen; Ya Fang Chen; Viswanadha Vijaya Padma; Ing Shiow Lay; Chih Yang Huang

doi:10.5603/CJ.a2016.0087

Enhancement of beta-catenin in cardiomyocytes suppresses survival protein expression but promotes apoptosis and fibrosis

James C. Lin, Wei Wen Kuo, Rathinasamy Baskaran, Ming Cheng Chen, Tsung Jung Ho, Ray Jade Chen, Ya Fang Chen, Viswanadha Vijaya Padma, Ing Shiow Lay, Chih Yang Huang

Research output: Contribution to journal › Article › peer-review

18 Citations (Scopus)

Abstract

Background: Beta-catenin has been implicated in cell-cell communication in a wide variety of developmental and physiological processes. Defective Wnt signaling could result in various cardiac and vascular abnormalities. Little is known regarding Wnt/frizzled pathway in cardiomyocyte apoptosis. Methods: In this study, the role of b-catenin in apoptosis was investigated in H9c2 cardiomyocytes and primary cardiomyocytes isolated in diabetic Wistar rats. The cardiomyocytes were transfected with porcine cytomegalovirus (pCMV)-b-catenin plasmid in order to overexpress b-catenin. Results: The transcription factor displayed a significant nuclear localization in Wistar rats with cardiac hypertension. Transfection of b-catenin plasmid induced apoptosis and reduced expression of survival pathway markers in cardiomyocytes in a dose-dependent manner. Furthermore, expression of fibrosis protein markers was upregulated by the overexpression. Conclusions: Taken together, these results revealed that altered Wnt/b-catenin signaling might provoke heart failure.

Original language	English
Pages (from-to)	195-205
Number of pages	11
Journal	Cardiology Journal
Volume	24
Issue number	2
DOIs	https://doi.org/10.5603/CJ.a2016.0087
Publication status	Published - 2017

Keywords

Apoptosis
Cardiomyocytes
Fibrosis
Survival pathway
β-catenin

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.5603/CJ.a2016.0087

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title = "Enhancement of beta-catenin in cardiomyocytes suppresses survival protein expression but promotes apoptosis and fibrosis",

abstract = "Background: Beta-catenin has been implicated in cell-cell communication in a wide variety of developmental and physiological processes. Defective Wnt signaling could result in various cardiac and vascular abnormalities. Little is known regarding Wnt/frizzled pathway in cardiomyocyte apoptosis. Methods: In this study, the role of b-catenin in apoptosis was investigated in H9c2 cardiomyocytes and primary cardiomyocytes isolated in diabetic Wistar rats. The cardiomyocytes were transfected with porcine cytomegalovirus (pCMV)-b-catenin plasmid in order to overexpress b-catenin. Results: The transcription factor displayed a significant nuclear localization in Wistar rats with cardiac hypertension. Transfection of b-catenin plasmid induced apoptosis and reduced expression of survival pathway markers in cardiomyocytes in a dose-dependent manner. Furthermore, expression of fibrosis protein markers was upregulated by the overexpression. Conclusions: Taken together, these results revealed that altered Wnt/b-catenin signaling might provoke heart failure.",

keywords = "Apoptosis, Cardiomyocytes, Fibrosis, Survival pathway, β-catenin",

author = "Lin, {James C.} and Kuo, {Wei Wen} and Rathinasamy Baskaran and Chen, {Ming Cheng} and Ho, {Tsung Jung} and Chen, {Ray Jade} and Chen, {Ya Fang} and Padma, {Viswanadha Vijaya} and Lay, {Ing Shiow} and Huang, {Chih Yang}",

note = "Funding Information: This study is supported in part by the Taiwan Ministry of Health and Welfare Clinical Trial and Research Center of Excellence (MOHW105-TDU--B-212-133019). Publisher Copyright: {\textcopyright} 2017 Via Medica.",

year = "2017",

doi = "10.5603/CJ.a2016.0087",

language = "English",

volume = "24",

pages = "195--205",

journal = "Cardiology Journal",

issn = "1897-5593",

publisher = "Via Medica",

number = "2",

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T1 - Enhancement of beta-catenin in cardiomyocytes suppresses survival protein expression but promotes apoptosis and fibrosis

AU - Lin, James C.

AU - Kuo, Wei Wen

AU - Baskaran, Rathinasamy

AU - Chen, Ming Cheng

AU - Ho, Tsung Jung

AU - Chen, Ray Jade

AU - Chen, Ya Fang

AU - Padma, Viswanadha Vijaya

AU - Lay, Ing Shiow

AU - Huang, Chih Yang

N1 - Funding Information: This study is supported in part by the Taiwan Ministry of Health and Welfare Clinical Trial and Research Center of Excellence (MOHW105-TDU--B-212-133019). Publisher Copyright: © 2017 Via Medica.

PY - 2017

Y1 - 2017

N2 - Background: Beta-catenin has been implicated in cell-cell communication in a wide variety of developmental and physiological processes. Defective Wnt signaling could result in various cardiac and vascular abnormalities. Little is known regarding Wnt/frizzled pathway in cardiomyocyte apoptosis. Methods: In this study, the role of b-catenin in apoptosis was investigated in H9c2 cardiomyocytes and primary cardiomyocytes isolated in diabetic Wistar rats. The cardiomyocytes were transfected with porcine cytomegalovirus (pCMV)-b-catenin plasmid in order to overexpress b-catenin. Results: The transcription factor displayed a significant nuclear localization in Wistar rats with cardiac hypertension. Transfection of b-catenin plasmid induced apoptosis and reduced expression of survival pathway markers in cardiomyocytes in a dose-dependent manner. Furthermore, expression of fibrosis protein markers was upregulated by the overexpression. Conclusions: Taken together, these results revealed that altered Wnt/b-catenin signaling might provoke heart failure.

AB - Background: Beta-catenin has been implicated in cell-cell communication in a wide variety of developmental and physiological processes. Defective Wnt signaling could result in various cardiac and vascular abnormalities. Little is known regarding Wnt/frizzled pathway in cardiomyocyte apoptosis. Methods: In this study, the role of b-catenin in apoptosis was investigated in H9c2 cardiomyocytes and primary cardiomyocytes isolated in diabetic Wistar rats. The cardiomyocytes were transfected with porcine cytomegalovirus (pCMV)-b-catenin plasmid in order to overexpress b-catenin. Results: The transcription factor displayed a significant nuclear localization in Wistar rats with cardiac hypertension. Transfection of b-catenin plasmid induced apoptosis and reduced expression of survival pathway markers in cardiomyocytes in a dose-dependent manner. Furthermore, expression of fibrosis protein markers was upregulated by the overexpression. Conclusions: Taken together, these results revealed that altered Wnt/b-catenin signaling might provoke heart failure.

KW - Apoptosis

KW - Cardiomyocytes

KW - Fibrosis

KW - Survival pathway

KW - β-catenin

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Enhancement of beta-catenin in cardiomyocytes suppresses survival protein expression but promotes apoptosis and fibrosis

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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