Yes-associated protein (YAP) mediates adaptive cardiac hypertrophy in response to pressure overload

Byun, Jaemin; Re, Dominic P. Del; Zhai, Peiyong; Ikeda, Shohei; Shirakabe, Akihiro; Mizushima, Wataru; Miyamoto, Shigeki; Brown, Joan Heller; Sadoshima, Junichi

doi:10.1074/jbc.ra118.006123

Cited by 75 publications

(72 citation statements)

References 53 publications

(73 reference statements)

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“…However, it should be noticed that gene therapy technology is still far from clinical application due to low organ specificity and other drawbacks 46 . Furthermore, sustained activation of YAP may lead to adaptive cardiac hypertrophy upon hypertrophic stress and lead to tumorigenesis in other organs 47,48 . If using progesterone as a therapy method, the duration and dosage can be well controlled, thus avoiding the side effects resulted from sustained and non‐specific YAP activation.…”

Section: Discussionmentioning

confidence: 99%

Progesterone, via yes‐associated protein, promotes cardiomyocyte proliferation and cardiac repair

Cao

Chen

et al. 2020

Cell Proliferation

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Objectives The mechanisms responsible for the postnatal loss of mammalian cardiac regenerative capacity are not fully elucidated. The aim of the present study is to investigate the role of progesterone in cardiac regeneration and explore underlying mechanism. Materials and Methods Effect of progesterone on cardiomyocyte proliferation was analysed by immunofluorescent staining. RNA sequencing was performed to screen key target genes of progesterone, and yes‐associated protein (YAP) was knocked down to demonstrate its role in pro‐proliferative effect of progesterone. Effect of progesterone on activity of YAP promoter was measured by luciferase assay and interaction between progesterone receptor and YAP promoter by electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP). Adult mice were subjected to myocardial infarction, and then, effects of progesterone on adult cardiac regeneration were analysed. Results Progesterone supplementation enhanced cardiomyocyte proliferation in a progesterone receptor‐dependent manner. Progesterone up‐regulated YAP expression and knockdown of YAP by small interfering RNA reduced progesterone‐mediated cardiomyocyte proliferative effect. Progesterone receptor interacted with the YAP promoter, determined by ChIP and EMSA; progesterone increased luciferase activity of YAP promoter and up‐regulated YAP target genes. Progesterone administration also promoted adult cardiomyocyte proliferation and improved cardiac function in myocardial infarction. Conclusion Our data uncover a role of circulating progesterone withdrawal as a novel mechanism for the postnatal loss of mammalian cardiac regenerative potential. Progesterone promotes both neonatal and adult cardiomyocyte proliferation by up‐regulating YAP expression.

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Section: Discussionmentioning

confidence: 99%

Progesterone, via yes‐associated protein, promotes cardiomyocyte proliferation and cardiac repair

Cao

Chen

et al. 2020

Cell Proliferation

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“…Cell cycle regulators, growth factors, and signaling through the Meis homeobox 1 (Meis1)-, Hippo/Yes-associated protein (YAP)-, switch/sucrose nonfermentable (SWI/SNF)-, neuregulin 1 (NRG1)-, and p38-pathway are proven to exert a fundamental role in cardiomyogenesis during postnatal development [47][48][49]. Furthermore, these factors also control hypertrophic growth of the adult mammalian myocardium in response to pressure overload [50][51][52][53][54][55][56]. These findings suggest that these cellular mechanisms are not only crucial to adapt to the changes during postnatal life but also allow adaptation to cellular stress during adulthood.…”

Section: Differences and Similarities In The Mechanisms Underlying Camentioning

confidence: 99%

Reviewing the Limitations of Adult Mammalian Cardiac Regeneration: Noncoding RNAs as Regulators of Cardiomyogenesis

2020

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The adult mammalian heart is incapable of regeneration following cardiac injury, leading to a decline in function and eventually heart failure. One of the most evident barriers limiting cardiac regeneration is the inability of cardiomyocytes to divide. It has recently become clear that the mammalian heart undergoes limited cardiomyocyte self-renewal throughout life and is even capable of modest regeneration early after birth. These exciting findings have awakened the goal to promote cardiomyogenesis of the human heart to repair cardiac injury or treat heart failure. We are still far from understanding why adult mammalian cardiomyocytes possess only a limited capacity to proliferate. Identifying the key regulators may help to progress towards such revolutionary therapy. Specific noncoding RNAs control cardiomyocyte division, including well explored microRNAs and more recently emerged long noncoding RNAs. Elucidating their function and molecular mechanisms during cardiomyogenesis is a prerequisite to advance towards therapeutic options for cardiac regeneration. In this review, we present an overview of the molecular basis of cardiac regeneration and describe current evidence implicating microRNAs and long noncoding RNAs in this process. Current limitations and future opportunities regarding how these regulatory mechanisms can be harnessed to study myocardial regeneration will be addressed.

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“…The nuclear and cytosolic-enriched fractions were prepared using NE-PER nuclear and cytoplasmic extraction kit (Pierce) according to the manufacturer's instructions (43). Western blotting was conducted following isolation of fractions.…”

Section: Nuclear Fractionationmentioning

confidence: 99%

The tumor suppressor RASSF1A modulates inflammation and injury in the reperfused murine myocardium

Francisco¹,

Byun²,

Kalloo

et al. 2019

Journal of Biological Chemistry

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Yes-associated protein (YAP) mediates adaptive cardiac hypertrophy in response to pressure overload

Cited by 75 publications

References 53 publications

Progesterone, via yes‐associated protein, promotes cardiomyocyte proliferation and cardiac repair

Progesterone, via yes‐associated protein, promotes cardiomyocyte proliferation and cardiac repair

Reviewing the Limitations of Adult Mammalian Cardiac Regeneration: Noncoding RNAs as Regulators of Cardiomyogenesis

The tumor suppressor RASSF1A modulates inflammation and injury in the reperfused murine myocardium

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