cells Article Cardiomyocyte-Specific Deletion of Orai1 Reveals Its Protective Role in Angiotensin-II-Induced Pathological Cardiac Remodeling Sebastian Segin 1,2, Michael Berlin 1,2, Christin Richter 1, Rebekka Medert 1,2, Veit Flockerzi 3, Paul Worley 4, Marc Freichel 1,2 and Juan E. Camacho Londoño 1,2,* 1 Pharmakologisches Institut, Ruprecht-Karls-Universität Heidelberg, INF 366, 69120 Heidelberg, Germany;
[email protected] (S.S.);
[email protected] (M.B.);
[email protected] (C.R.);
[email protected] (R.M.);
[email protected] (M.F.) 2 DZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, 69120 Heidelberg, Germany 3 Experimentelle und Klinische Pharmakologie und Toxikologie, Universität des Saarlandes, 66421 Homburg, Germany;
[email protected] 4 The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA;
[email protected] * Correspondence:
[email protected]; Tel.: +49-6221-54-86863; Fax: +49-6221-54-8644 Received: 26 March 2020; Accepted: 24 April 2020; Published: 28 April 2020 Abstract: Pathological cardiac remodeling correlates with chronic neurohumoral stimulation and abnormal Ca2+ signaling in cardiomyocytes. Store-operated calcium entry (SOCE) has been described in adult and neonatal murine cardiomyocytes, and Orai1 proteins act as crucial ion-conducting constituents of this calcium entry pathway that can be engaged not only by passive Ca2+ store depletion but also by neurohumoral stimuli such as angiotensin-II. In this study, we, therefore, analyzed the consequences of Orai1 deletion for cardiomyocyte hypertrophy in neonatal and adult cardiomyocytes as well as for other features of pathological cardiac remodeling including cardiac contractile function in vivo.