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Calcium Handling
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Calcium Handling

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 13508

Special Issue Editor

Dr. Demetrios A. Arvanitis

E-Mail Website
Guest Editor
Center of Basic Research, Biomedical Research Foundation of the Academy of Athens, 115 27 Athens, Greece
Interests: cell biology; physiology; genetics; calcium, cardiomyocytes; neurons
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Calcium ion (Ca2+) handling is the central coordinator of excitable cell functions. For neuronal, skeletal, cardiac or smooth muscle, and pancreatic beta cells, transient elevation of intracellular Ca2+ triggers molecular machines and produces key cellular responses, such as contraction and secretion. This is mediated through the maintenance of the resting cytosolic Ca2+ concentration, four orders of magnitude lower than the extracellular space and three orders of magnitude lower than the endoplasmic reticulum or the mitochondria. Upon excitation, these Ca2+ stores release Ca2+ to the cytosol through ion channels, while during relaxation, ATPase pumps reuptake cytosolic Ca2+ to its stores. These channels and pumps are under the control of accessory proteins that modify their function upon extracellular or intracellular signaling. Genetic variations, protein modifications, and expression changes of the molecules involved have been associated with human diseases. Targeting druggable Ca2+ handling proteins may serve as therapy for neuronal, skeletal muscle, and cardiac or endocrinal diseases. This Issue of IJMS (“Calcium Handling”) presents novel research and reviews in the field of Ca2+ handling proteins’ molecular interplay and regulation in cell physiology and pathophysiology.

Dr. Demetrios A. Arvanitis
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • Ca2+
  • endoplasmic reticulum
  • mitochondria
  • neurons
  • skeletal muscle
  • cardiac muscle
  • smooth muscle
  • pancreatic beta cells
  • contractility
  • secretion

Related Special Issue

Published Papers (5 papers)

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Research

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9 pages, 2984 KiB  
Communication
Dilated-Left Ventricular Non-Compaction Cardiomyopathy in a Pediatric Case with SPEG Compound Heterozygous Variants
by Hager Jaouadi, Fedoua El Louali, Chloé Wanert, Aline Cano, Caroline Ovaert and Stéphane Zaffran
Int. J. Mol. Sci. 2022, 23(9), 5205; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23095205 - 06 May 2022
Cited by 1 | Viewed by 1585
Abstract
Left Ventricular Non-Compaction (LVNC) is defined by the triad prominent myocardial trabecular meshwork, thin compacted layer, and deep intertrabecular recesses. LVNC associated with dilation is characterized by the coexistence of left ventricular dilation and systolic dysfunction. Pediatric cases with dilated-LVNC have worse outcomes [...] Read more.
Left Ventricular Non-Compaction (LVNC) is defined by the triad prominent myocardial trabecular meshwork, thin compacted layer, and deep intertrabecular recesses. LVNC associated with dilation is characterized by the coexistence of left ventricular dilation and systolic dysfunction. Pediatric cases with dilated-LVNC have worse outcomes than those with isolated dilated cardiomyopathy and adult patients. Herein, we report a clinical and genetic investigation using trio-based whole-exome sequencing of a pediatric case with early-onset dilated-LVNC. Compound heterozygous mutations were identified in the Striated Muscle Enriched Protein Kinase (SPEG) gene, a key regulator of cardiac calcium homeostasis. A paternally inherited mutation: SPEG; p.(Arg2470Ser) and the second variant, SPEG; p.(Pro2687Thr), is common and occurred de novo. Subsequently, Sanger sequencing was performed for the family in order to segregate the variants. Thus, the index case, his father, and both sisters carried the SPEG: p.(Arg2470Ser) variant. Only the index patient carried both SPEG variants. Both sisters, as well as the patient’s father, showed LVNC without cardiac dysfunction. The unaffected mother did not harbor any of the variants. The in silico analysis of the identified variants (rare and common) showed a decrease in protein stability with alterations of the physical properties as well as high conservation scores for the mutated residues. Interestingly, using the Project HOPE tool, the SPEG; p.(Pro2687Thr) variant is predicted to disturb the second fibronectin type III domain of the protein and may abolish its function. To our knowledge, the present case is the first description of compound heterozygous SPEG mutations involving a de novo variant and causing dilated-LVNC without neuropathy or centronuclear myopathy. Full article
(This article belongs to the Special Issue Calcium Handling)
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11 pages, 2080 KiB  
Article
Augmented KCa2.3 Channel Feedback Regulation of Oxytocin Stimulated Uterine Strips from Nonpregnant Mice
by Megan Zak, Bri Kestler, Trudy Cornwell and Mark S. Taylor
Int. J. Mol. Sci. 2021, 22(24), 13585; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222413585 - 18 Dec 2021
Cited by 4 | Viewed by 2011
Abstract
Uterine contractions prior to 37 weeks gestation can result in preterm labor with significant risk to the infant. Current tocolytic therapies aimed at suppressing premature uterine contractions are largely ineffective and cause serious side effects. Calcium (Ca2+) dependent contractions of uterine [...] Read more.
Uterine contractions prior to 37 weeks gestation can result in preterm labor with significant risk to the infant. Current tocolytic therapies aimed at suppressing premature uterine contractions are largely ineffective and cause serious side effects. Calcium (Ca2+) dependent contractions of uterine smooth muscle are physiologically limited by the opening of membrane potassium (K+) channels. Exploiting such inherent negative feedback mechanisms may offer new strategies to delay labor and reduce risk. Positive modulation of small conductance Ca2+-activated K+ (KCa2.3) channels with cyclohexyl-[2-(3,5-dimethyl-pyrazol-1-yl)-6-methyl-pyrimidin-4-yl]-amine (CyPPA), effectively decreases uterine contractions. This study investigates whether the receptor agonist oxytocin might solicit KCa2.3 channel feedback that facilitates CyPPA suppression of uterine contractions. Using isometric force myography, we found that spontaneous phasic contractions of myometrial tissue from nonpregnant mice were suppressed by CyPPA and, in the presence of CyPPA, oxytocin failed to augment contractions. In tissues exposed to oxytocin, depletion of internal Ca2+ stores with cyclopiazonic acid (CPA) impaired CyPPA relaxation, whereas blockade of nonselective cation channels (NSCC) using gadolinium (Gd3+) had no significant effect. Immunofluorescence revealed close proximity of KCa2.3 channels and ER inositol trisphosphate receptors (IP3Rs) within myometrial smooth muscle cells. The findings suggest internal Ca2+ stores play a role in KCa2.3-dependent feedback control of uterine contraction and offer new insights for tocolytic therapies. Full article
(This article belongs to the Special Issue Calcium Handling)
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17 pages, 3684 KiB  
Communication
Time-Dependent Image Restoration of Low-SNR Live-Cell Ca2 Fluorescence Microscopy Data
by Lena-Marie Woelk, Sukanya A. Kannabiran , Valerie J. Brock , Christine E. Gee , Christian Lohr , Andreas H. Guse , Björn-Philipp Diercks  and René Werner
Int. J. Mol. Sci. 2021, 22(21), 11792; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222111792 - 30 Oct 2021
Cited by 6 | Viewed by 2185
Abstract
Live-cell Ca2+ fluorescence microscopy is a cornerstone of cellular signaling analysis and imaging. The demand for high spatial and temporal imaging resolution is, however, intrinsically linked to a low signal-to-noise ratio (SNR) of the acquired spatio-temporal image data, which impedes on [...] Read more.
Live-cell Ca2+ fluorescence microscopy is a cornerstone of cellular signaling analysis and imaging. The demand for high spatial and temporal imaging resolution is, however, intrinsically linked to a low signal-to-noise ratio (SNR) of the acquired spatio-temporal image data, which impedes on the subsequent image analysis. Advanced deconvolution and image restoration algorithms can partly mitigate the corresponding problems but are usually defined only for static images. Frame-by-frame application to spatio-temporal image data neglects inter-frame contextual relationships and temporal consistency of the imaged biological processes. Here, we propose a variational approach to time-dependent image restoration built on entropy-based regularization specifically suited to process low- and lowest-SNR fluorescence microscopy data. The advantage of the presented approach is demonstrated by means of four datasets: synthetic data for in-depth evaluation of the algorithm behavior; two datasets acquired for analysis of initial Ca2+ microdomains in T-cells; finally, to illustrate the transferability of the methodical concept to different applications, one dataset depicting spontaneous Ca2+ signaling in jGCaMP7b-expressing astrocytes. To foster re-use and reproducibility, the source code is made publicly available. Full article
(This article belongs to the Special Issue Calcium Handling)
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16 pages, 6999 KiB  
Article
Passive Transfer of Blood Sera from ALS Patients with Identified Mutations Results in Elevated Motoneuronal Calcium Level and Loss of Motor Neurons in the Spinal Cord of Mice
by Tamás F. Polgár, Valéria Meszlényi, Bernát Nógrádi, Laura Körmöczy, Krisztina Spisák, Kornélia Tripolszki, Márta Széll, Izabella Obál, József I. Engelhardt, László Siklós and Roland Patai
Int. J. Mol. Sci. 2021, 22(18), 9994; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22189994 - 16 Sep 2021
Cited by 4 | Viewed by 1867
Abstract
Introduction: Previously, we demonstrated the degeneration of axon terminals in mice after repeated injections of blood sera from amyotrophic lateral sclerosis (ALS) patients with identified mutations. However, whether a similar treatment affects the cell body of motor neurons (MNs) remained unresolved. Methods: Sera [...] Read more.
Introduction: Previously, we demonstrated the degeneration of axon terminals in mice after repeated injections of blood sera from amyotrophic lateral sclerosis (ALS) patients with identified mutations. However, whether a similar treatment affects the cell body of motor neurons (MNs) remained unresolved. Methods: Sera from healthy individuals or ALS patients with a mutation in different ALS-related genes were intraperitoneally injected into ten-week-old male Balb/c mice (n = 3/serum) for two days. Afterward, the perikaryal calcium level was measured using electron microscopy. Furthermore, the optical disector method was used to evaluate the number of lumbar MNs. Results: The cytoplasmic calcium level of the lumbar MNs of the ALS-serum-treated mice, compared to untreated and healthy-serum-treated controls, was significantly elevated. While injections of the healthy serum did not reduce the number of MNs compared to the untreated control group, ALS sera induced a remarkable loss of MNs. Discussion: Similarly to the distant motor axon terminals, the injection of blood sera of ALS patients has a rapid degenerative effect on MNs. Analogously, the magnitude of the evoked changes was specific to the type of mutation; furthermore, the degeneration was most pronounced in the group treated with sera from ALS patients with a mutation in the chromosome 9 open reading frame 72 gene. Full article
(This article belongs to the Special Issue Calcium Handling)
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Review

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22 pages, 4609 KiB  
Review
Calcium and Heart Failure: How Did We Get Here and Where Are We Going?
by Natthaphat Siri-Angkul, Behzad Dadfar, Riya Jaleel, Jazna Naushad, Jaseela Parambathazhath, Angelia A. Doye, Lai-Hua Xie and Judith K. Gwathmey
Int. J. Mol. Sci. 2021, 22(14), 7392; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22147392 - 09 Jul 2021
Cited by 10 | Viewed by 4529
Abstract
The occurrence and prevalence of heart failure remain high in the United States as well as globally. One person dies every 30 s from heart disease. Recognizing the importance of heart failure, clinicians and scientists have sought better therapeutic strategies and even cures [...] Read more.
The occurrence and prevalence of heart failure remain high in the United States as well as globally. One person dies every 30 s from heart disease. Recognizing the importance of heart failure, clinicians and scientists have sought better therapeutic strategies and even cures for end-stage heart failure. This exploration has resulted in many failed clinical trials testing novel classes of pharmaceutical drugs and even gene therapy. As a result, along the way, there have been paradigm shifts toward and away from differing therapeutic approaches. The continued prevalence of death from heart failure, however, clearly demonstrates that the heart is not simply a pump and instead forces us to consider the complexity of simplicity in the pathophysiology of heart failure and reinforces the need to discover new therapeutic approaches. Full article
(This article belongs to the Special Issue Calcium Handling)
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