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Cells
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Calcium Signaling in Skeletal and Cardiac Health and Diseases
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Calcium Signaling in Skeletal and Cardiac Health and Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (5 July 2022) | Viewed by 14398

Special Issue Editors

Dr. Jessica Sabourin

E-Mail Website
Guest Editor
Signalling and Cardiovascular Pathophysiology, Faculty of pharmacy, INSERM UMR-S 1180-LABEX LERMIT, 92296 Châtenay-Malabry, France
Interests: physiology; heart; cell biology; calcium signaling; skeletal muscle; cardiac arrhythmias; calcium channels, store-operated Ca2+ channels
Dr. Jean-Pierre Benitah

E-Mail Website
Guest Editor
Signalling and Cardiovascular Pathophysiology, Faculty of pharmacy, INSERM UMR-S 1180-LABEX LERMIT, 92296 Châtenay-Malabry, France
Interests: Ca2+ channels; ryanodine receptor; store-operated Ca2+ entry’ excitation-contraction coupling; excitation-transcription coupling; arrhythmia; hypertrophy; heart failure

Special Issue Information

Dear Colleagues,

The spatiotemporal modulation of intracellular Ca2+ levels provides a signal transduction mechanism in virtually all cell types. This is used to determine which short- and long-term cellular functions are activated and when. Ion channels, pumps, and exchangers in the plasma membrane and/or endoplasmic/sarcoplasmic reticulum are responsible for this fine control of Ca2+ handling. Nonetheless, several important skeletal and cardiac disease states result from abnormal remodeling of Ca2+ signaling. This Special Issue welcomes manuscripts providing insight on aspects relevant to calcium signaling in skeletal and cardiac health and diseases.

Dr. Jessica Sabourin
Dr. Jean-Pierre Benitah
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • calcium handling
  • calcium channels
  • pumps and exchangers
  • mitochondria and calcium
  • sarcoplasmic reticulum and calcium
  • excitation-contraction coupling
  • skeletal disease
  • cardiac disease
  • calcium remodeling

Published Papers (5 papers)

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Research

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18 pages, 2591 KiB  
Article
Reduction in SOCE and Associated Aggregation in Platelets from Mice with Platelet-Specific Deletion of Orai1
by Linlin Yang, Roger Ottenheijm, Paul Worley, Marc Freichel and Juan E. Camacho Londoño
Cells 2022, 11(20), 3225; https://doi.org/10.3390/cells11203225 - 14 Oct 2022
Cited by 3 | Viewed by 1615
Abstract
Calcium signalling in platelets through store operated Ca2+ entry (SOCE) or receptor-operated Ca2+ entry (ROCE) mechanisms is crucial for platelet activation and function. Orai1 proteins have been implicated in platelet’s SOCE. In this study we evaluated the contribution of Orai1 proteins [...] Read more.
Calcium signalling in platelets through store operated Ca2+ entry (SOCE) or receptor-operated Ca2+ entry (ROCE) mechanisms is crucial for platelet activation and function. Orai1 proteins have been implicated in platelet’s SOCE. In this study we evaluated the contribution of Orai1 proteins to these processes using washed platelets from adult mice from both genders with platelet-specific deletion of the Orai1 gene (Orai1flox/flox; Pf4-Cre termed as Orai1Plt-KO) since mice with ubiquitous Orai1 deficiency show early lethality. Platelet aggregation as well as Ca2+ entry and release were measured in vitro following stimulation with collagen, collagen related peptide (CRP), thromboxane A2 analogue U46619, thrombin, ADP and the sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) inhibitor thapsigargin, respectively. SOCE and aggregation induced by Thapsigargin up to a concentration of 0.3 µM was abrogated in Orai1-deficient platelets. Receptor-operated Ca2+-entry and/or platelet aggregation induced by CRP, U46619 or thrombin were partially affected by Orai1 deletion depending on the gender. In contrast, ADP-, collagen- and CRP-induced aggregation was comparable in Orai1Plt-KO platelets and control cells over the entire concentration range. Our results reinforce the indispensability of Orai1 proteins for SOCE in murine platelets, contribute to understand its role in agonist-dependent signalling and emphasize the importance to analyse platelets from both genders. Full article
(This article belongs to the Special Issue Calcium Signaling in Skeletal and Cardiac Health and Diseases)
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14 pages, 2700 KiB  
Article
Oxygen Consumption and Basal Metabolic Rate as Markers of Susceptibility to Malignant Hyperthermia and Heat Stroke
by Matteo Serano, Laura Pietrangelo, Cecilia Paolini, Flavia A. Guarnier and Feliciano Protasi
Cells 2022, 11(16), 2468; https://doi.org/10.3390/cells11162468 - 9 Aug 2022
Cited by 5 | Viewed by 2414
Abstract
Calsequestrin 1 (CASQ1) and Ryanodine receptor 1 (RYR1) are two of the main players in excitation–contraction (EC) coupling. CASQ1-knockout mice and mice carrying a mutation in RYR1 (Y522S) linked to human malignant hyperthermia susceptibility (MHS) both suffer lethal hypermetabolic episodes when exposed to [...] Read more.
Calsequestrin 1 (CASQ1) and Ryanodine receptor 1 (RYR1) are two of the main players in excitation–contraction (EC) coupling. CASQ1-knockout mice and mice carrying a mutation in RYR1 (Y522S) linked to human malignant hyperthermia susceptibility (MHS) both suffer lethal hypermetabolic episodes when exposed to halothane (MHS crises) and to environmental heat (heat stroke, HS). The phenotype of Y522S is more severe than that of CASQ1-null mice. As MHS and HS are hypermetabolic responses, we studied the metabolism of adult CASQ1-null and Y522S mice using wild-type (WT) mice as controls. We found that CASQ1-null and Y522S mice have increased food consumption and higher core temperature at rest. By indirect calorimetry, we then verified that CASQ1-null and Y522S mice show an increased oxygen consumption and a lower respiratory quotient (RQ). The accelerated metabolism of CASQ1-null and Y522S mice was also accompanied with a reduction in body fat. Moreover, both mouse models displayed increased oxygen consumption and a higher core temperature during heat stress. The results collected suggest that metabolic rate, oxygen consumption, and body temperature at rest, all more elevated in Y522S than in CASQ1-null mice, could possibly be used as predictors of the level of susceptibility to hyperthermic crises of mice (and possibly humans). Full article
(This article belongs to the Special Issue Calcium Signaling in Skeletal and Cardiac Health and Diseases)
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15 pages, 1412 KiB  
Article
Regulation of APD and Force by the Na+/Ca2+ Exchanger in Human-Induced Pluripotent Stem Cell-Derived Engineered Heart Tissue
by Djemail Ismaili, Katrin Gurr, András Horváth, Lei Yuan, Marc D. Lemoine, Carl Schulz, Jascha Sani, Johannes Petersen, Hermann Reichenspurner, Paulus Kirchhof, Thomas Jespersen, Thomas Eschenhagen, Arne Hansen, Jussi T. Koivumäki and Torsten Christ
Cells 2022, 11(15), 2424; https://doi.org/10.3390/cells11152424 - 5 Aug 2022
Cited by 4 | Viewed by 2945
Abstract
The physiological importance of NCX in human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) is not well characterized but may depend on the relative strength of the current, compared to adult cardiomyocytes, and on the exact spatial arrangement of proteins involved in Ca2+ extrusion. [...] Read more.
The physiological importance of NCX in human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) is not well characterized but may depend on the relative strength of the current, compared to adult cardiomyocytes, and on the exact spatial arrangement of proteins involved in Ca2+ extrusion. Here, we determined NCX currents and its contribution to action potential and force in hiPSC-CMs cultured in engineered heart tissue (EHT). The results were compared with data from rat and human left ventricular tissue. The NCX currents in hiPSC-CMs were larger than in ventricular cardiomyocytes isolated from human left ventricles (1.3 ± 0.2 pA/pF and 3.2 ± 0.2 pA/pF for human ventricle and EHT, respectively, p < 0.05). SEA0400 (10 µM) markedly shortened the APD90 in EHT (by 26.6 ± 5%, p < 0.05) and, to a lesser extent, in rat ventricular tissue (by 10.7 ± 1.6%, p < 0.05). Shortening in human left ventricular preparations was small and not different from time-matched controls (TMCs; p > 0.05). Force was increased by the NCX block in rat ventricle (by 31 ± 5.4%, p < 0.05) and EHT (by 20.8 ± 3.9%, p < 0.05), but not in human left ventricular preparations. In conclusion, hiPSC-CMs possess NCX currents not smaller than human left ventricular tissue. Robust NCX block-induced APD shortening and inotropy makes EHT an attractive pharmacological model. Full article
(This article belongs to the Special Issue Calcium Signaling in Skeletal and Cardiac Health and Diseases)
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15 pages, 2802 KiB  
Article
Global PIEZO1 Gain-of-Function Mutation Causes Cardiac Hypertrophy and Fibrosis in Mice
by Fiona Bartoli, Elizabeth L. Evans, Nicola M. Blythe, Leander Stewart, Eulashini Chuntharpursat-Bon, Marjolaine Debant, Katie E. Musialowski, Laeticia Lichtenstein, Gregory Parsonage, T. Simon Futers, Neil A. Turner and David J. Beech
Cells 2022, 11(7), 1199; https://doi.org/10.3390/cells11071199 - 2 Apr 2022
Cited by 14 | Viewed by 4501
Abstract
PIEZO1 is a subunit of mechanically-activated, nonselective cation channels. Gain-of-function PIEZO1 mutations are associated with dehydrated hereditary stomatocytosis (DHS), a type of anaemia, due to abnormal red blood cell function. Here, we hypothesised additional effects on the heart. Consistent with this hypothesis, mice [...] Read more.
PIEZO1 is a subunit of mechanically-activated, nonselective cation channels. Gain-of-function PIEZO1 mutations are associated with dehydrated hereditary stomatocytosis (DHS), a type of anaemia, due to abnormal red blood cell function. Here, we hypothesised additional effects on the heart. Consistent with this hypothesis, mice engineered to contain the M2241R mutation in PIEZO1 to mimic a DHS mutation had increased cardiac mass and interventricular septum thickness at 8–12 weeks of age, without altered cardiac contractility. Myocyte size was greater and there was increased expression of genes associated with cardiac hypertrophy (Anp, Acta1 and β-MHC). There was also cardiac fibrosis, increased expression of Col3a1 (a gene associated with fibrosis) and increased responses of isolated cardiac fibroblasts to PIEZO1 agonism. The data suggest detrimental effects of excess PIEZO1 activity on the heart, mediated in part by amplified PIEZO1 function in cardiac fibroblasts. Full article
(This article belongs to the Special Issue Calcium Signaling in Skeletal and Cardiac Health and Diseases)
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Review

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19 pages, 552 KiB  
Review
The SOCE Machinery: An Unbalanced Knowledge between Left and Right Ventricular Pathophysiology
by Jessica Sabourin, Antoine Beauvais, Rui Luo, David Montani, Jean-Pierre Benitah, Bastien Masson and Fabrice Antigny
Cells 2022, 11(20), 3282; https://doi.org/10.3390/cells11203282 - 18 Oct 2022
Cited by 6 | Viewed by 2086
Abstract
Right ventricular failure (RVF) is the most important prognostic factor for morbidity and mortality in pulmonary arterial hypertension (PAH) or pulmonary hypertension (PH) caused by left heart diseases. However, right ventricle (RV) remodeling is understudied and not targeted by specific therapies. This can [...] Read more.
Right ventricular failure (RVF) is the most important prognostic factor for morbidity and mortality in pulmonary arterial hypertension (PAH) or pulmonary hypertension (PH) caused by left heart diseases. However, right ventricle (RV) remodeling is understudied and not targeted by specific therapies. This can be partly explained by the lack of basic knowledge of RV remodeling. Since the physiology and hemodynamic function of the RV differ from those of the left ventricle (LV), the mechanisms of LV dysfunction cannot be generalized to that of the RV, albeit a knowledge of these being helpful to understanding RV remodeling and dysfunction. Store-operated Ca2+ entry (SOCE) has recently emerged to participate in the LV cardiomyocyte Ca2+ homeostasis and as a critical player in Ca2+ mishandling in a pathological context. In this paper, we highlight the current knowledge on the SOCE contribution to the LV and RV dysfunctions, as SOCE molecules are present in both compartments. he relative lack of studies on RV dysfunction indicates the necessity of further investigations, a significant challenge over the coming years. Full article
(This article belongs to the Special Issue Calcium Signaling in Skeletal and Cardiac Health and Diseases)
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