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  The focal adhesion protein beta-parvin controls cardiomyocyte shape and sarcomere assembly in response to mechanical load

Thievessen, I., Suhr, F., Vergarajauregui, S., Böttcher, R. T., Brixius, K., Rosenberger, G., et al. (2022). The focal adhesion protein beta-parvin controls cardiomyocyte shape and sarcomere assembly in response to mechanical load. Current Biology, 32(14), 3033-3047. doi:10.1016/j.cub.2022.05.047.

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 Creators:
Thievessen, Ingo1, Author           
Suhr, Frank, Author
Vergarajauregui, Silvia, Author
Böttcher, Ralph T.1, Author           
Brixius, Klara, Author
Rosenberger, Georg, Author
Dewald, Oliver, Author
Fleischmann, Bernd K., Author
Ghanem, Alexander, Author
Kruger, Marcus2, Author           
Engel, Felix B.2, Author           
Fabry, Ben, Author
Bloch, Wilhelm, Author
Fässler, Reinhard1, Author           
Affiliations:
1Fässler, Reinhard / Molecular Medicine, Max Planck Institute of Biochemistry, Max Planck Society, ou_1565147              
2Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591695              

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Free keywords: INTEGRIN-LINKED KINASE; MYOCYTE-SPECIFIC EXCISION; RAT VENTRICULAR MYOCYTES; PRESSURE-OVERLOAD; CARDIAC-HYPERTROPHY; MEMBRANE PROTRUSIONS; CELL MORPHOLOGY; HEART-FAILURE; ALPHA-PIX; ILKBiochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology;
 Abstract: Physiological and pathological cardiac stress induced by exercise and hypertension, respectively, increase the hemodynamic load for the heart and trigger specific hypertrophic signals in cardiomyocytes leading to adaptive or maladaptive cardiac hypertrophy responses involving a mechanosensitive remodeling of the contractile cytoskeleton. Integrins sense load and have been implicated in cardiac hypertrophy, but how they discriminate between the two types of cardiac stress and translate mechanical loads into specific cytoskeletal signaling pathways is not clear Here, we report that the focal adhesion protein beta-parvin is highly expressed in cardiomyocytes and facilitates the formation of cell protrusions, the serial assembly of newly synthesized sarcomeres, and the hypertrophic growth of neonatal rat ventricular cardiomyocytes (NRVCs) in vitro. In addition, physiological mechanical loading of NRVCs by either the application of cyclic, uni-axial stretch, or culture on physiologically stiff substrates promotes NRVC elongation in a beta-parvin-dependent manner, which is achieved by binding of beta-parvin to alpha/beta-PIX, which in turn activates Rac1. Importantly, loss-of-function studies in mice also revealed that beta-parvin is essential for the exercise-induced cardiac hypertrophy response in vivo. Our results identify beta-parvin as a novel mechano-responsive signaling hub in hypertrophic cardiomyocytes that drives cell elongation in response to physiological mechanical loads.

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Language(s): eng - English
 Dates: 2022-07-25
 Publication Status: Issued
 Pages: 25
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: ISI: 000842373000018
DOI: 10.1016/j.cub.2022.05.047
 Degree: -

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Title: Current Biology
  Abbreviation : Curr. Biol.
Source Genre: Journal
 Creator(s):
Affiliations:
Publ. Info: London, UK : Cell Press
Pages: - Volume / Issue: 32 (14) Sequence Number: - Start / End Page: 3033 - 3047 Identifier: ISSN: 0960-9822
CoNE: https://pure.mpg.de/cone/journals/resource/954925579107