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Advances in Calcium Signaling
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Advances in Calcium Signaling

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

Deadline for manuscript submissions: closed (15 August 2022) | Viewed by 13306

Special Issue Editor

Dr. Md Shahidul Islam

E-Mail Website
Guest Editor
1. Department of Clinical Sciences and Education, Sodersjukhuset, Karolinska Institutet, 118 83 Stockholm, Sweden
2. Department of Emergency Care and Internal Medicine, Uppsala University Hospital, 752 37 Uppsala, Sweden
Interests: islets of Langerhans; pancreatic beta cells; insulin secretion; glucagon-like peptide 1; calcium signaling; TRP channels; diabetes; signal transduction in beta-cells; stimulus-secretion coupling; calcium signaling in the beta cells; calcium-induced calcium release; ryanodine receptors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This special issue will contain original research articles and comprehensive reviews that deal with any of the diverse aspects of calcium signaling in any cell systems. Any aspect of the broad field of calcium signaling including the mechanisms of generation and decoding of calcium signals; ion-channels, pumps, transporters, membranes, organelle, binding-proteins, receptors, kinases-phosphatases, receptors, genes and modelling approaches in calcium signaling could be of interest. The roles of calcium signaling in mediating cellular functions like exocytosis, neurotransmission, growth, differentiation, oncogenesis, and disease processes will be included in this issue. Manuscripts on translational research in the field of calcium signaling will be of special interest.   

Dr. Md Shahidul Islam
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. 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.

Published Papers (6 papers)

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Research

Jump to: Review

16 pages, 3878 KiB  
Article
Dynamic Balance between PTH1R-Dependent Signal Cascades Determines Its Pro- or Anti-Osteogenic Effects on MSC
by Konstantin Kulebyakin, Pyotr Tyurin-Kuzmin, Leila Sozaeva, Nikita Voloshin, Mikhail Nikolaev, Vadim Chechekhin, Maxim Vigovskiy, Veronika Sysoeva, Elizaveta Korchagina, Daria Naida and Maria Vorontsova
Cells 2022, 11(21), 3519; https://doi.org/10.3390/cells11213519 - 07 Nov 2022
Cited by 4 | Viewed by 1987
Abstract
Parathyroid hormone (PTH) is one of the key regulators of calcium and phosphate metabolism in the body, controlling bone metabolism and ion excretion by the kidneys. At present, attempts to use PTH as a therapeutic agent have been associated with side-effects, the nature [...] Read more.
Parathyroid hormone (PTH) is one of the key regulators of calcium and phosphate metabolism in the body, controlling bone metabolism and ion excretion by the kidneys. At present, attempts to use PTH as a therapeutic agent have been associated with side-effects, the nature of which is not always clear and predictable. In addition, it is known that in vivo impairment of PTH post-receptor signaling is associated with atypical differentiation behavior not only of bone cells, but also of connective tissues, including adipose tissue. In this work, we studied the functional responses of multipotent mesenchymal stromal cells (MSCs) to the action of PTH at the level of single cells. We used MSCs isolated from the periosteum and subcutaneous adipose tissue to compare characteristics of cell responses to PTH. We found that the hormone can activate three key responses via its receptor located on the surface of MSCs: single transients of calcium, calcium oscillations, and hormone-activated smooth increase in intracellular calcium. These types of calcium responses led to principally different cellular responses of MSCs. The cAMP-dependent smooth increase of intracellular calcium was associated with pro-osteogenic action of PTH, whereas phospholipase C dependent calcium oscillations led to a decrease in osteogenic differentiation intensity. Different variants of calcium responses are in dynamic equilibrium. Suppression of one type of response leads to increased activation of another type and, accordingly, to a change in the effect of PTH on cell differentiation. Full article
(This article belongs to the Special Issue Advances in Calcium Signaling)
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17 pages, 3070 KiB  
Article
Calcium-Related Genes Predicting Outcomes and Serving as Therapeutic Targets in Endometrial Cancer
by Ting Huang, Xuan Feng, Jiaqi Wang, Jingyi Zhou and Jianliu Wang
Cells 2022, 11(19), 3156; https://doi.org/10.3390/cells11193156 - 08 Oct 2022
Cited by 2 | Viewed by 1955
Abstract
Endometrial cancer (EC) is the most common gynecologic cancer with increasing incidence. The dysregulation of intracellular calcium plays a crucial role in cancer progression. However, the relationship between calcium-related genes and prognosis remains unclear. In this study, we aimed to establish a risk [...] Read more.
Endometrial cancer (EC) is the most common gynecologic cancer with increasing incidence. The dysregulation of intracellular calcium plays a crucial role in cancer progression. However, the relationship between calcium-related genes and prognosis remains unclear. In this study, we aimed to establish a risk model based on calcium-related genes for prognosis prediction in patients with EC. The TCGA-total set was divided into a training set and a testing set (1:1). The four-gene prognostic signature (CACNA2D1, SLC8A1, TRPM4 and CCL2) was established and classified all EC patients into a low-risk or high-risk group. This model was validated in both the testing dataset and the total set. The EC patients with high RiskScores showed significantly shorter overall survival than those with low RiskScores, and this trend was consistent among most subgroups. Moreover, an enrichment analysis confirmed that calcium-related and estrogen-response signalings were significantly enriched in the high-risk group. The knockdown of CACNA2D1 by siRNA or its blocker, amlodipine (AM) inhibited cell proliferation and induced cycle arrest in vitro. The calcium channel blocker AM inhibited cell proliferation and induced cycle arrest in vitro. AM also showed marked tumor inhibition effects in vivo. In summary, the prognostic model constructed by four calcium-related genes can reliably predict the outcomes of EC patients, and a calcium channel blocker, AM, has significant potential for EC treatment. Full article
(This article belongs to the Special Issue Advances in Calcium Signaling)
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18 pages, 3353 KiB  
Article
PKC-Mediated Orai1 Channel Phosphorylation Modulates Ca2+ Signaling in HeLa Cells
by Ericka Martínez-Martínez, Víctor Hugo Sánchez-Vázquez, Daniel León-Aparicio, Jose Sanchez-Collado, Martín-Leonardo Gallegos-Gómez, Juan A. Rosado, Juan M. Arias and Agustin Guerrero-Hernández
Cells 2022, 11(13), 2037; https://doi.org/10.3390/cells11132037 - 27 Jun 2022
Cited by 3 | Viewed by 2595
Abstract
The overexpression of the Orai1 channel inhibits SOCE when using the Ca2+ readdition protocol. However, we found that HeLa cells overexpressing the Orai1 channel displayed enhanced Ca2+ entry and a limited ER depletion in response to the combination of ATP and [...] Read more.
The overexpression of the Orai1 channel inhibits SOCE when using the Ca2+ readdition protocol. However, we found that HeLa cells overexpressing the Orai1 channel displayed enhanced Ca2+ entry and a limited ER depletion in response to the combination of ATP and thapsigargin (TG) in the presence of external Ca2+. As these effects require the combination of an agonist and TG, we decided to study whether the phosphorylation of Orai1 S27/S30 residues had any role using two different mutants: Orai1-S27/30A (O1-AA, phosphorylation-resistant) and Orai1-S27/30D (O1-DD, phosphomimetic). Both O1-wt and O1-AA supported enhanced Ca2+ entry, but this was not the case with O1-E106A (dead-pore mutant), O1-DD, and O1-AA-E106A, while O1-wt, O1-E106A, and O1-DD inhibited the ATP and TG-induced reduction of ER [Ca2+], suggesting that the phosphorylation of O1 S27/30 interferes with the IP3R activity. O1-wt and O1-DD displayed an increased interaction with IP3R in response to ATP and TG; however, the O1-AA channel decreased this interaction. The expression of mCherry-O1-AA increased the frequency of ATP-induced sinusoidal [Ca2+]i oscillations, while mCherry-O1-wt and mCherry-O1-DD decreased this frequency. These data suggest that the combination of ATP and TG stimulates Ca2+ entry, and the phosphorylation of Orai1 S27/30 residues by PKC reduces IP3R-mediated Ca2+ release. Full article
(This article belongs to the Special Issue Advances in Calcium Signaling)
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21 pages, 3672 KiB  
Article
Critical Requirements for the Initiation of a Cardiac Arrhythmia in Rat Ventricle: How Many Myocytes?
by Aman Ullah, Minh Tuan Hoang-Trong, William Jonathan Lederer, Raimond L. Winslow and Mohsin Saleet Jafri
Cells 2022, 11(12), 1878; https://doi.org/10.3390/cells11121878 - 09 Jun 2022
Cited by 3 | Viewed by 1760
Abstract
Cardiovascular disease is the leading cause of death worldwide due in a large part to arrhythmia. In order to understand how calcium dynamics play a role in arrhythmogenesis, normal and dysfunctional Ca2+ signaling in a subcellular, cellular, and tissued level is examined [...] Read more.
Cardiovascular disease is the leading cause of death worldwide due in a large part to arrhythmia. In order to understand how calcium dynamics play a role in arrhythmogenesis, normal and dysfunctional Ca2+ signaling in a subcellular, cellular, and tissued level is examined using cardiac ventricular myocytes at a high temporal and spatial resolution using multiscale computational modeling. Ca2+ sparks underlie normal excitation–contraction coupling. However, under pathological conditions, Ca2+ sparks can combine to form Ca2+ waves. These propagating elevations of (Ca2+)i can activate an inward Na+–Ca2+ exchanger current (INCX) that contributes to early after-depolarization (EADs) and delayed after-depolarizations (DADs). However, how cellular currents lead to full depolarization of the myocardium and how they initiate extra systoles is still not fully understood. This study explores how many myocytes must be entrained to initiate arrhythmogenic depolarizations in biophysically detailed computational models. The model presented here suggests that only a small number of myocytes must activate in order to trigger an arrhythmogenic propagating action potential. These conditions were examined in 1-D, 2-D, and 3-D considering heart geometry. The depolarization of only a few hundred ventricular myocytes is required to trigger an ectopic depolarization. The number decreases under disease conditions such as heart failure. Furthermore, in geometrically restricted parts of the heart such as the thin muscle strands found in the trabeculae and papillary muscle, the number of cells needed to trigger a propagating depolarization falls even further to less than ten myocytes. Full article
(This article belongs to the Special Issue Advances in Calcium Signaling)
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19 pages, 3603 KiB  
Article
Taste Cells of the Type III Employ CASR to Maintain Steady Serotonin Exocytosis at Variable Ca2+ in the Extracellular Medium
by Aleksandr P. Cherkashin, Olga A. Rogachevskaja, Natalia V. Kabanova, Polina D. Kotova, Marina F. Bystrova and Stanislav S. Kolesnikov
Cells 2022, 11(8), 1369; https://doi.org/10.3390/cells11081369 - 18 Apr 2022
Cited by 2 | Viewed by 2136
Abstract
Type III taste cells are the only taste bud cells which express voltage-gated (VG) Ca2+ channels and employ Ca2+-dependent exocytosis to release neurotransmitters, particularly serotonin. The taste bud is a tightly packed cell population, wherein extracellular Ca2+ is expected [...] Read more.
Type III taste cells are the only taste bud cells which express voltage-gated (VG) Ca2+ channels and employ Ca2+-dependent exocytosis to release neurotransmitters, particularly serotonin. The taste bud is a tightly packed cell population, wherein extracellular Ca2+ is expected to fluctuate markedly due to the electrical activity of taste cells. It is currently unclear whether the Ca2+ entry-driven synapse in type III cells could be reliable enough at unsteady extracellular Ca2. Here we assayed depolarization-induced Ca2+ signals and associated serotonin release in isolated type III cells at varied extracellular Ca2+. It turned out that the same depolarizing stimulus elicited invariant Ca2+ signals in type III cells irrespective of bath Ca2+ varied within 0.5–5 mM. The serotonin release from type III cells was assayed with the biosensor approach by using HEK-293 cells co-expressing the recombinant 5-HT4 receptor and genetically encoded cAMP sensor Pink Flamindo. Consistently with the weak Ca2+ dependence of intracellular Ca2+ transients produced by VG Ca2+ entry, depolarization-triggered serotonin secretion varied negligibly with bath Ca2+. The evidence implicated the extracellular Ca2+-sensing receptor in mediating the negative feedback mechanism that regulates VG Ca2+ entry and levels off serotonin release in type III cells at deviating Ca2+ in the extracellular medium. Full article
(This article belongs to the Special Issue Advances in Calcium Signaling)
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Review

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13 pages, 814 KiB  
Review
Recent Developments on the Roles of Calcium Signals and Potential Therapy Targets in Cervical Cancer
by Jiahui Lei, Fengying Deng, Hongmei Ding, Mengyu Fu, Ting Xu, Bingyu Ji, Lin Feng, Min Li, Junlan Qiu and Qinqin Gao
Cells 2022, 11(19), 3003; https://doi.org/10.3390/cells11193003 - 26 Sep 2022
Cited by 5 | Viewed by 1765
Abstract
Intracellular calcium (Ca2+) concentration ([Ca2+]i) is implicated in proliferation, invasion, and metastasis in cancerous tissues. A variety of oncologic therapies and some candidate drugs induce their antitumor effects (in part or in whole) through the modulation of [Ca2+ [...] Read more.
Intracellular calcium (Ca2+) concentration ([Ca2+]i) is implicated in proliferation, invasion, and metastasis in cancerous tissues. A variety of oncologic therapies and some candidate drugs induce their antitumor effects (in part or in whole) through the modulation of [Ca2+]i. Cervical cancer is one of most common cancers among women worldwide. Recently, major research advances relating to the Ca2+ signals in cervical cancer are emerging. In this review, we comprehensively describe the current progress concerning the roles of Ca2+ signals in the occurrence, development, and prognosis of cervical cancer. It will enhance our understanding of the causative mechanism of Ca2+ signals in cervical cancer and thus provide new sights for identifying potential therapeutic targets for drug discovery. Full article
(This article belongs to the Special Issue Advances in Calcium Signaling)
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