Blockade of Fibroblast YAP Attenuates Cardiac Fibrosis and Dysfunction Through MRTF-A Inhibition

[Display omitted] •YAP is activated by myocardial infarction or neuroendocrine stimulation in cardiac fibroblasts.•Active YAP promotes TEA domain transcription factor-1–mediated transcription of myocardin-related transcription factor A to facilitate cardiac myofibroblast differentiation and extracel...

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Published in:	JACC. Basic to translational science Vol. 5; no. 9; pp. 931 - 945
Main Authors:	Francisco, Jamie, Zhang, Yu, Jeong, Jae Im, Mizushima, Wataru, Ikeda, Shohei, Ivessa, Andreas, Oka, Shinichi, Zhai, Peiyong, Tallquist, Michelle D., Del Re, Dominic P.
Format:	Journal Article
Language:	English
Published:	United States Elsevier Inc 01.09.2020 Elsevier
Subjects:	cardiac fibrosis Cardiovascular heart failure Hippo signaling myocardial infarction Preclinical Research YAP heart failure Hippo signaling NRCF MRTF-A SMA myocardial infarction Mkl1 YAP mRNA TGF TEAD cardiac fibrosis PE MCM PDGFR MI AngII myocardin-related transcription factor A neonatal rat cardiac fibroblast Mer-Cre-Mer phenylephrine platelet-derived growth factor receptor messenger ribonucleic acid yes-associated protein megakaryoblastic leukemia 1 TEA domain transcription factor angiotensin II transforming growth factor smooth muscle actin NRCF, neonatal rat cardiac fibroblast MRTF-A, myocardin-related transcription factor A Mkl1, megakaryoblastic leukemia 1 YAP, yes-associated protein MI, myocardial infarction PDGFR, platelet-derived growth factor receptor SMA, smooth muscle actin TGF, transforming growth factor MCM, Mer-Cre-Mer PE, phenylephrine AngII, angiotensin II TEAD, TEA domain transcription factor mRNA, messenger ribonucleic acid
ISSN:	2452-302X, 2452-302X
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Abstract	[Display omitted] •YAP is activated by myocardial infarction or neuroendocrine stimulation in cardiac fibroblasts.•Active YAP promotes TEA domain transcription factor-1–mediated transcription of myocardin-related transcription factor A to facilitate cardiac myofibroblast differentiation and extracellular matrix gene expression.•Cardiac fibroblast YAP knockout mice have attenuated cardiac fibrosis and dysfunction in response to myocardial infarction. Fibrotic remodeling of the heart in response to injury contributes to heart failure, yet therapies to treat fibrosis remain elusive. Yes-associated protein (YAP) is activated in cardiac fibroblasts by myocardial infarction, and genetic inhibition of fibroblast YAP attenuates myocardial infarction–induced cardiac dysfunction and fibrosis. YAP promotes myofibroblast differentiation and associated extracellular matrix gene expression through engagement of TEA domain transcription factor 1 and subsequent de novo expression of myocardin-related transcription factor A. Thus, fibroblast YAP is a promising therapeutic target to prevent fibrotic remodeling and heart failure.
AbstractList	[Display omitted] •YAP is activated by myocardial infarction or neuroendocrine stimulation in cardiac fibroblasts.•Active YAP promotes TEA domain transcription factor-1–mediated transcription of myocardin-related transcription factor A to facilitate cardiac myofibroblast differentiation and extracellular matrix gene expression.•Cardiac fibroblast YAP knockout mice have attenuated cardiac fibrosis and dysfunction in response to myocardial infarction. Fibrotic remodeling of the heart in response to injury contributes to heart failure, yet therapies to treat fibrosis remain elusive. Yes-associated protein (YAP) is activated in cardiac fibroblasts by myocardial infarction, and genetic inhibition of fibroblast YAP attenuates myocardial infarction–induced cardiac dysfunction and fibrosis. YAP promotes myofibroblast differentiation and associated extracellular matrix gene expression through engagement of TEA domain transcription factor 1 and subsequent de novo expression of myocardin-related transcription factor A. Thus, fibroblast YAP is a promising therapeutic target to prevent fibrotic remodeling and heart failure. • YAP is activated by myocardial infarction or neuroendocrine stimulation in cardiac fibroblasts. • Active YAP promotes TEA domain transcription factor-1–mediated transcription of myocardin-related transcription factor A to facilitate cardiac myofibroblast differentiation and extracellular matrix gene expression. • Cardiac fibroblast YAP knockout mice have attenuated cardiac fibrosis and dysfunction in response to myocardial infarction. Fibrotic remodeling of the heart in response to injury contributes to heart failure, yet therapies to treat fibrosis remain elusive. Yes-associated protein (YAP) is activated in cardiac fibroblasts by myocardial infarction, and genetic inhibition of fibroblast YAP attenuates myocardial infarction–induced cardiac dysfunction and fibrosis. YAP promotes myofibroblast differentiation and associated extracellular matrix gene expression through engagement of TEA domain transcription factor 1 and subsequent de novo expression of myocardin-related transcription factor A. Thus, fibroblast YAP is a promising therapeutic target to prevent fibrotic remodeling and heart failure. Fibrotic remodeling of the heart in response to injury contributes to heart failure, yet therapies to treat fibrosis remain elusive. Yes-associated protein (YAP) is activated in cardiac fibroblasts by myocardial infarction, and genetic inhibition of fibroblast YAP attenuates myocardial infarction-induced cardiac dysfunction and fibrosis. YAP promotes myofibroblast differentiation and associated extracellular matrix gene expression through engagement of TEA domain transcription factor 1 and subsequent de novo expression of myocardin-related transcription factor A. Thus, fibroblast YAP is a promising therapeutic target to prevent fibrotic remodeling and heart failure. Fibrotic remodeling of the heart in response to injury contributes to heart failure, yet therapies to treat fibrosis remain elusive. Yes-associated protein (YAP) is activated in cardiac fibroblasts by myocardial infarction, and genetic inhibition of fibroblast YAP attenuates myocardial infarction-induced cardiac dysfunction and fibrosis. YAP promotes myofibroblast differentiation and associated extracellular matrix gene expression through engagement of TEA domain transcription factor 1 and subsequent de novo expression of myocardin-related transcription factor A. Thus, fibroblast YAP is a promising therapeutic target to prevent fibrotic remodeling and heart failure.Fibrotic remodeling of the heart in response to injury contributes to heart failure, yet therapies to treat fibrosis remain elusive. Yes-associated protein (YAP) is activated in cardiac fibroblasts by myocardial infarction, and genetic inhibition of fibroblast YAP attenuates myocardial infarction-induced cardiac dysfunction and fibrosis. YAP promotes myofibroblast differentiation and associated extracellular matrix gene expression through engagement of TEA domain transcription factor 1 and subsequent de novo expression of myocardin-related transcription factor A. Thus, fibroblast YAP is a promising therapeutic target to prevent fibrotic remodeling and heart failure. Visual Abstract
Author	Mizushima, Wataru Tallquist, Michelle D. Del Re, Dominic P. Zhang, Yu Ikeda, Shohei Oka, Shinichi Jeong, Jae Im Ivessa, Andreas Francisco, Jamie Zhai, Peiyong
Author_xml	– sequence: 1 givenname: Jamie surname: Francisco fullname: Francisco, Jamie organization: Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, New Jersey, USA – sequence: 2 givenname: Yu surname: Zhang fullname: Zhang, Yu organization: Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, New Jersey, USA – sequence: 3 givenname: Jae Im surname: Jeong fullname: Jeong, Jae Im organization: Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, New Jersey, USA – sequence: 4 givenname: Wataru surname: Mizushima fullname: Mizushima, Wataru organization: Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, New Jersey, USA – sequence: 5 givenname: Shohei surname: Ikeda fullname: Ikeda, Shohei organization: Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, New Jersey, USA – sequence: 6 givenname: Andreas surname: Ivessa fullname: Ivessa, Andreas organization: Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, New Jersey, USA – sequence: 7 givenname: Shinichi surname: Oka fullname: Oka, Shinichi organization: Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, New Jersey, USA – sequence: 8 givenname: Peiyong surname: Zhai fullname: Zhai, Peiyong organization: Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, New Jersey, USA – sequence: 9 givenname: Michelle D. surname: Tallquist fullname: Tallquist, Michelle D. organization: Center for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, Hawaii, USA – sequence: 10 givenname: Dominic P. surname: Del Re fullname: Del Re, Dominic P. email: delredo@njms.rutgers.edu organization: Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, New Jersey, USA
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Keywords	heart failure Hippo signaling NRCF MRTF-A SMA myocardial infarction Mkl1 YAP mRNA TGF TEAD cardiac fibrosis PE MCM PDGFR MI AngII myocardin-related transcription factor A neonatal rat cardiac fibroblast Mer-Cre-Mer phenylephrine platelet-derived growth factor receptor messenger ribonucleic acid yes-associated protein megakaryoblastic leukemia 1 TEA domain transcription factor angiotensin II transforming growth factor smooth muscle actin NRCF, neonatal rat cardiac fibroblast MRTF-A, myocardin-related transcription factor A Mkl1, megakaryoblastic leukemia 1 YAP, yes-associated protein MI, myocardial infarction PDGFR, platelet-derived growth factor receptor SMA, smooth muscle actin TGF, transforming growth factor MCM, Mer-Cre-Mer PE, phenylephrine AngII, angiotensin II TEAD, TEA domain transcription factor mRNA, messenger ribonucleic acid
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Snippet	[Display omitted] •YAP is activated by myocardial infarction or neuroendocrine stimulation in cardiac fibroblasts.•Active YAP promotes TEA domain transcription... Visual Abstract Fibrotic remodeling of the heart in response to injury contributes to heart failure, yet therapies to treat fibrosis remain elusive. Yes-associated protein... • YAP is activated by myocardial infarction or neuroendocrine stimulation in cardiac fibroblasts. • Active YAP promotes TEA domain transcription...
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SubjectTerms	cardiac fibrosis Cardiovascular heart failure Hippo signaling myocardial infarction Preclinical Research YAP
Title	Blockade of Fibroblast YAP Attenuates Cardiac Fibrosis and Dysfunction Through MRTF-A Inhibition
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