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Genetic Catalytic Inactivation of GRK5 Impairs Cardiac Function in Mice Via Dysregulated P53 Levels
Marzano, Federica Liccardo, Daniela Elia, Andrea Mucio, Ines de Lucia, Claudio Lucchese, Anna Maria Gao, Erhe Ferrara, Nicola Rapacciuolo, Antonio Paolocci, Nazareno
Marzano, Federica
Liccardo, Daniela
Elia, Andrea
Mucio, Ines
de Lucia, Claudio
Lucchese, Anna Maria
Gao, Erhe
Ferrara, Nicola
Rapacciuolo, Antonio
Paolocci, Nazareno
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Journal article
Date
2022-04-25
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Pharmacology
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http://dx.doi.org/10.1016/j.jacbts.2022.01.001
Abstract
GRK5’s catalytic activity in regulating basal and stressed cardiac function has not been studied. Herein, we studied knock-in mice in which GRK5 was mutated to render it catalytically inactive (K215R). At baseline, GRK5-K215R mice showed a marked decline in cardiac function with increased apoptosis and fibrosis. In vitro, restriction of GRK5 inside the nucleus of cardiomyocytes resulted in enhanced cell death along with higher p53 levels. Moreover, in fibroblasts, we demonstrated that K215R mutation promoted the transition into myofibroblast phenotype. This study provides novel insight into the biological actions of GRK5, that are essential for its future targeting.
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Citation
Federica Marzano, Daniela Liccardo, Andrea Elia, Ines Mucio, Claudio de Lucia, Anna Maria Lucchese, Erhe Gao, Nicola Ferrara, Antonio Rapacciuolo, Nazareno Paolocci, Giuseppe Rengo, Walter J. Koch, Alessandro Cannavo, Genetic Catalytic Inactivation of GRK5 Impairs Cardiac Function in Mice Via Dysregulated P53 Levels, JACC: Basic to Translational Science, Volume 7, Issue 4, 2022, Pages 366-380, ISSN 2452-302X, https://doi.org/10.1016/j.jacbts.2022.01.001.
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Elsevier
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JACC: Basic to Translational Science, Vol. 7, Iss. 4
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