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.
Authors
- Ioannis Akoumianakis (ORCID: https://orcid.org/0000-0002-4674-0210)
- Neel Mehta (ORCID: https://orcid.org/0000-0001-6143-9840)
- Svetlana Reilly (ORCID: https://orcid.org/0000-0003-1231-1239)
- Violetta Steeples (ORCID: https://orcid.org/0000-0002-5468-460X)
- Rana A Sayeed (ORCID: https://orcid.org/0000-0002-2887-1874)
- Hugh Watkins (ORCID: https://orcid.org/0000-0002-5287-9016)
- Carmen Töpfer
- Leticia Moreira (ORCID: https://orcid.org/0000-0002-4518-8591)
- Alexander J. Sparrow (ORCID: https://orcid.org/0000-0002-3354-3314)
- George Krasopoulos (ORCID: https://orcid.org/0000-0001-9334-9604)
- Stanley Nattel (ORCID: https://orcid.org/0000-0002-5565-3311)
- Charles Redwood (ORCID: https://orcid.org/0000-0002-8673-7542)
- Paul Robinson (ORCID: https://orcid.org/0000-0002-3918-4420)
- Charalambos Antoniades
- K A Agon
Institutions
- Montreal Heart Institute (CA)
- John Radcliffe Hospital (GB)
- University of Oxford (GB)
Publication Details
- 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
- Field-Weighted Citation Impact
- 0.00