Calcitonin signalling system regulates function and arhythmogenicity of atrial cardiomyocytes

Abstract Background Atrial fibrillation (AF) poses a significant therapeutic challenge due to myocardial remodelling, involving both structural and electrical alterations. Recent investigations have shed light on the role of atrial cardiomyocytes (CMs) in secreting Calcitonin (CT), a factor crucial for maintaining atrial tissue integrity. Dysregulated CT secretion in AF showed to contribute to fibrotic tissue production by atrial fibroblasts, exacerbating arrhythmogenesis [1]. However, the direct impact of CT on CM function and arrhythmogenicity remains unclear, driving the objectives of our study. Methods/Results Serum samples from 20 cardiac surgery patients revealed a noteworthy association between higher pre-operative CT levels and a significant ~2.8-fold reduction in the incidence of post-operative AF (poAF). Using freshly isolated atrial guinea pig CMs, confirmed (by qPCR and immunofluorescence) that CMs express CT-receptor (CTR) to enable CT actions in the cell. Functional studies found that CT administration inhibits spontaneous calcium (Ca2+)-release events induced by pacing and decreases the Ca2+ transients amplitude (at 2 Hz; IonOptix μstep system) in fura2-loaded CMs (n=22 cells) in a concentration-dependent manner. Atrial iPSC-CMs transduced with global RGECO sensor (Genetically encoded Ca2+ indicator) and treated with 15 pM CT showed a reduction in the beat rate when paced at 2Hz, and a significantly increased the time to 50% baseline. Evaluation of the expression and phosphorylation of selected Ca2+ handling proteins, which may potentially account for the observed changes in Ca2+ transients, showed no differences in total or phospho-(ser2808) ryanodine receptor, and SERCA2α in response to CT but an increase in phospho-(Ser16) Phospholamban. Conclusion Our findings highlight the effects of CT on atrial CM function. Maintaining physiological CT levels offer a promising approach for managing AF clinically, potentially through the use of already in clinical use CT-analogues.

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Journal
European Heart Journal
Published
2024-10-01
DOI
https://doi.org/10.1093/eurheartj/ehae666.3775
Primary Topic
Signaling Pathways in Disease
Type
article
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article

Calcitonin signalling system regulates function and arhythmogenicity of atrial cardiomyocytes

Ioannis Akoumianakis, Neel Mehta, Svetlana Reilly, Violetta Steeples et al.
European Heart Journal
Signaling Pathways in Disease
article

Calcitonin signalling system regulates function and arhythmogenicity of atrial cardiomyocytes

Ioannis Akoumianakis, Neel Mehta, Svetlana Reilly, Violetta Steeples, Rana A Sayeed, Hugh Watkins, Carmen Töpfer, Leticia Moreira, Alexander J. Sparrow, George Krasopoulos, Stanley Nattel, Charles Redwood, Paul Robinson, Charalambos Antoniades, K A Agon
article en

Abstract

Abstract Background Atrial fibrillation (AF) poses a significant therapeutic challenge due to myocardial remodelling, involving both structural and electrical alterations. Recent investigations have shed light on the role of atrial cardiomyocytes (CMs) in secreting Calcitonin (CT), a factor crucial for maintaining atrial tissue integrity. Dysregulated CT secretion in AF showed to contribute to fibrotic tissue production by atrial fibroblasts, exacerbating arrhythmogenesis [1]. However, the direct impact of CT on CM function and arrhythmogenicity remains unclear, driving the objectives of our study. Methods/Results Serum samples from 20 cardiac surgery patients revealed a noteworthy association between higher pre-operative CT levels and a significant ~2.8-fold reduction in the incidence of post-operative AF (poAF). Using freshly isolated atrial guinea pig CMs, confirmed (by qPCR and immunofluorescence) that CMs express CT-receptor (CTR) to enable CT actions in the cell. Functional studies found that CT administration inhibits spontaneous calcium (Ca2+)-release events induced by pacing and decreases the Ca2+ transients amplitude (at 2 Hz; IonOptix μstep system) in fura2-loaded CMs (n=22 cells) in a concentration-dependent manner. Atrial iPSC-CMs transduced with global RGECO sensor (Genetically encoded Ca2+ indicator) and treated with 15 pM CT showed a reduction in the beat rate when paced at 2Hz, and a significantly increased the time to 50% baseline. Evaluation of the expression and phosphorylation of selected Ca2+ handling proteins, which may potentially account for the observed changes in Ca2+ transients, showed no differences in total or phospho-(ser2808) ryanodine receptor, and SERCA2α in response to CT but an increase in phospho-(Ser16) Phospholamban. Conclusion Our findings highlight the effects of CT on atrial CM function. Maintaining physiological CT levels offer a promising approach for managing AF clinically, potentially through the use of already in clinical use CT-analogues.

European Heart JournalVol. 45(Supplement_1)
Montreal Heart Institute (CA), John Radcliffe Hospital (GB), University of Oxford (GB)
Openalex Percentile: Top 83%
Signaling Pathways in Disease
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