ArticleJournal of molecular and cellular cardiology2010
Cardiac-specific, inducible ClC-3 gene deletion eliminates native volume-sensitive chloride channels and produces myocardial hypertrophy in adult mice.
Article in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 51 citations in OpenAlex.
- Electrophysiological and Molecular Mechanisms of Sinoatrial Node Mechanosensitivity.Frontiers in cardiovascular medicine · 2021Article
- SVFX: a machine learning framework to quantify the pathogenicity of structural variants.Genome biology · 2020Article
- Dystrophin and calcium current are decreased in cardiomyocytes expressing Cre enzyme driven by αMHC but not TNT promoter.Scientific reports · 2019Article
- Caveolae-Mediated Activation of Mechanosensitive Chloride Channels in Pulmonary Veins Triggers Atrial Arrhythmogenesis.Journal of the American Heart Association · 2019Article
- Molecular biomarkers in cardiac hypertrophy.Journal of cellular and molecular medicine · 2019Review
- MiR-1-3p that correlates with left ventricular function of HCM can serve as a potential target and differentiate HCM from DCM.Journal of translational medicine · 2018Article
- ClC-3 Chloride Channel Proteins Regulate the Cell Cycle by Up-regulating cyclin D1-CDK4/6 through Suppressing p21/p27 Expression in Nasopharyngeal Carcinoma Cells.Scientific reports · 2016Article
- The impact of Cystic Fibrosis Transmembrane Regulator Disruption on cardiac function and stress response.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2016Article
- Increase in hypotonic stress-induced endocytic activity in macrophages via ClC-3.Molecules and cells · 2014Article
- Overexpression of myocardin induces partial transdifferentiation of human-induced pluripotent stem cell-derived mesenchymal stem cells into cardiomyocytes.Physiological reports · 2014Article
- ClC-3 is an intracellular chloride/proton exchanger with large voltage-dependent nonlinear capacitance.ACS chemical neuroscience · 2013Article
- Phenomics of cardiac chloride channels.Comprehensive Physiology · 2013Review
- Article
- Lost in transgenesis: a user's guide for genetically manipulating the mouse in cardiac research.Circulation research · 2012Review
- Systolic dysfunction in cardiac-specific ligand-inducible MerCreMer transgenic mice.American journal of physiology. Heart and circulatory physiology · 2011Article
- The ClC-3 chloride channels in cardiovascular disease.Acta pharmacologica Sinica · 2011Review
- Volume-sensitive chloride channels are involved in maintenance of basal cell volume in human acute lymphoblastic leukemia cells.The Journal of membrane biology · 2011Article
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
Native volume-sensitive outwardly rectifying anion channels (VSOACs) play a significant role in cell volume homeostasis in mammalian cells. However, the molecular correlate of VSOACs has been elusive to identify. The short isoform of ClC-3 (sClC-3) is a member of the mammalian ClC gene family and has been proposed to be a molecular candidate for VSOACs in cardiac myocytes and vascular smooth muscle cells. To directly test this hypothesis, and assess the physiological role of ClC-3 in cardiac function, we generated a novel line of cardiac-specific inducible ClC-3 knock-out mice. These transgenic mice were maintained on a doxycycline diet to preserve ClC-3 expression; removal of doxycycline activates Cre recombinase to inactivate the Clcn3 gene. Echocardiography revealed dramatically reduced ejection fraction and fractional shortening, and severe signs of myocardial hypertrophy and heart failure in the knock-out mice at both 1.5 and 3 weeks off doxycycline. In mice off doxycycline, time-dependent inactivation of ClC-3 gene expression was confirmed in atrial and ventricular cells by qRT-PCR and Western blot analysis. Electrophysiological examination of native VSOACs in isolated atrial and ventricular myocytes 3 weeks off doxycycline revealed a complete elimination of the currents, whereas at 1.5 weeks, VSOAC current densities were significantly reduced, compared to age-matched control mice maintained on doxycycline. These results indicate that ClC-3 is a key component of native VSOACs in mammalian heart and plays a significant cardioprotective role against cardiac hypertrophy and failure.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.