ArticleThe Journal of biological chemistry2012
Activation of transient receptor potential canonical 3 (TRPC3)-mediated Ca2+ entry by A1 adenosine receptor in cardiomyocytes disturbs atrioventricular conduction.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- The SOCE Machinery: An Unbalanced Knowledge between Left and Right Ventricular Pathophysiology.Cells · 2022Review
- Increase in PKCα Activity during Heart Failure Despite the Stimulation of PKCα Braking Mechanism.International journal of molecular sciences · 2020Article
- TRPC Channels: Dysregulation and CaCells · 2020Review
- Role of Transient Receptor Potential Canonical Channels in Heart Physiology and Pathophysiology.Frontiers in cardiovascular medicine · 2020Review
- TRP Channels: Current Perspectives in the Adverse Cardiac Remodeling.Frontiers in physiology · 2019Review
- AMolecular neurobiology · 2017Review
- Adenosine AAmerican journal of physiology. Renal physiology · 2017Article
- Transient Receptor Potential Canonical (TRPC)/Orai1-dependent Store-operated Ca2+ Channels: NEW TARGETS OF ALDOSTERONE IN CARDIOMYOCYTES.The Journal of biological chemistry · 2016Article
- Store-operated Ca2+ Entry Mediated by Orai1 and TRPC1 Participates to Insulin Secretion in Rat β-Cells.The Journal of biological chemistry · 2015Article
- Evidence of a Role for Fibroblast Transient Receptor Potential Canonical 3 Ca2+ Channel in Renal Fibrosis.Journal of the American Society of Nephrology : JASN · 2015Article
- A hypoxic episode during cardiogenesis downregulates the adenosinergic system and alters the myocardial anoxic tolerance.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Article
- Role of TRP channels in the cardiovascular system.American journal of physiology. Heart and circulatory physiology · 2015Review
- Editorial: Ca(2+) Signaling and Heart Rhythm.Frontiers in physiology · 2015Article
- The involvement of TRPC3 channels in sinoatrial arrhythmias.Frontiers in physiology · 2015Article
- Adenosine inhibits renin release from juxtaglomerular cells via an A1 receptor-TRPC-mediated pathway.American journal of physiology. Renal physiology · 2013Article
- Microarray-Based Comparisons of Ion Channel Expression Patterns: Human Keratinocytes to Reprogrammed hiPSCs to Differentiated Neuronal and Cardiac Progeny.Stem cells international · 2013Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the activation of the A(1)-subtype of the adenosine receptors (A(1)AR) is arrhythmogenic in the developing heart, little is known about the underlying downstream mechanisms. The aim of this study was to determine to what extent the transient receptor potential canonical (TRPC) channel 3, functioning as receptor-operated channel (ROC), contributes to the A(1)AR-induced conduction disturbances. Using embryonic atrial and ventricular myocytes obtained from 4-day-old chick embryos, we found that the specific activation of A(1)AR by CCPA induced sarcolemmal Ca(2+) entry. However, A(1)AR stimulation did not induce Ca(2+) release from the sarcoplasmic reticulum. Specific blockade of TRPC3 activity by Pyr3, by a dominant negative of TRPC3 construct, or inhibition of phospholipase Cs and PKCs strongly inhibited the A(1)AR-enhanced Ca(2+) entry. Ca(2+) entry through TRPC3 was activated by the 1,2-diacylglycerol (DAG) analog OAG via PKC-independent and -dependent mechanisms in atrial and ventricular myocytes, respectively. In parallel, inhibition of the atypical PKCζ by myristoylated PKCζ pseudosubstrate inhibitor significantly decreased the A(1)AR-enhanced Ca(2+) entry in both types of myocytes. Additionally, electrocardiography showed that inhibition of TRPC3 channel suppressed transient A(1)AR-induced conduction disturbances in the embryonic heart. Our data showing that A(1)AR activation subtly mediates a proarrhythmic Ca(2+) entry through TRPC3-encoded ROC by stimulating the phospholipase C/DAG/PKC cascade provide evidence for a novel pathway whereby Ca(2+) entry and cardiac function are altered. Thus, the A(1)AR-TRPC3 axis may represent a potential therapeutic target.
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