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Article

SH3-Binding Glutamic Acid Rich-Deficiency Augments Apoptosis in Neonatal Rat Cardiomyocytes

1
Department of Internal Medicine III, Cardiology and Angiology, University Medical Center Schleswig-Holstein, Campus Kiel, 24105 Kiel, Germany
2
Department of Cardiology, Angiology and Pneumology, University Hospital Heidelberg, 69120 Heidelberg, Germany
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DZHK (German Centre for Cardiovascular Research), Partner Site Hamburg/Kiel/Lübeck, 24105 Kiel, Germany
4
DZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, 69120 Heidelberg, Germany
*
Author to whom correspondence should be addressed.
Academic Editors: Nicole Wagner and Kay-Dietrich Wagner
Int. J. Mol. Sci. 2021, 22(20), 11042; https://doi.org/10.3390/ijms222011042
Received: 9 August 2021 / Revised: 5 October 2021 / Accepted: 8 October 2021 / Published: 13 October 2021
(This article belongs to the Special Issue Transcriptional Regulation of Cardiac Development and Disease)
Congenital heart disease (CHD) is one of the most common birth defects in humans, present in around 40% of newborns with Down’s syndrome (DS). The SH3 domain-binding glutamic acid-rich (SH3BGR) gene, which maps to the DS region, belongs to a gene family encoding a cluster of small thioredoxin-like proteins sharing SH3 domains. Although its expression is confined to the cardiac and skeletal muscle, the physiological role of SH3BGR in the heart is poorly understood. Interestingly, we observed a significant upregulation of SH3BGR in failing hearts of mice and human patients with hypertrophic cardiomyopathy. Along these lines, the overexpression of SH3BGR exhibited a significant increase in the expression of hypertrophic markers (Nppa and Nppb) and increased cell surface area in neonatal rat ventricular cardiomyocytes (NRVCMs), whereas its knockdown attenuated cellular hypertrophy. Mechanistically, using serum response factor (SRF) response element-driven luciferase assays in the presence or the absence of RhoA or its inhibitor, we found that the pro-hypertrophic effects of SH3BGR are mediated via the RhoA–SRF axis. Furthermore, SH3BGR knockdown resulted in the induction of apoptosis and reduced cell viability in NRVCMs via apoptotic Hippo–YAP signaling. Taking these results together, we here show that SH3BGR is vital for maintaining cytoskeletal integrity and cellular viability in NRVCMs through its modulation of the SRF/YAP signaling pathways. View Full-Text
Keywords: SH3BGR; cardiac hypertrophy; SRF signaling; Hippo signaling; apoptosis SH3BGR; cardiac hypertrophy; SRF signaling; Hippo signaling; apoptosis
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MDPI and ACS Style

Deshpande, A.; Borlepawar, A.; Rosskopf, A.; Frank, D.; Frey, N.; Rangrez, A.Y. SH3-Binding Glutamic Acid Rich-Deficiency Augments Apoptosis in Neonatal Rat Cardiomyocytes. Int. J. Mol. Sci. 2021, 22, 11042. https://doi.org/10.3390/ijms222011042

AMA Style

Deshpande A, Borlepawar A, Rosskopf A, Frank D, Frey N, Rangrez AY. SH3-Binding Glutamic Acid Rich-Deficiency Augments Apoptosis in Neonatal Rat Cardiomyocytes. International Journal of Molecular Sciences. 2021; 22(20):11042. https://doi.org/10.3390/ijms222011042

Chicago/Turabian Style

Deshpande, Anushka, Ankush Borlepawar, Alexandra Rosskopf, Derk Frank, Norbert Frey, and Ashraf Y. Rangrez 2021. "SH3-Binding Glutamic Acid Rich-Deficiency Augments Apoptosis in Neonatal Rat Cardiomyocytes" International Journal of Molecular Sciences 22, no. 20: 11042. https://doi.org/10.3390/ijms222011042

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