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Calcium Signaling in Health and Diseases

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

Deadline for manuscript submissions: closed (20 October 2024) | Viewed by 9565

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Special Issue Editors

Dr. Carlos Villalobos

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Instituto de Biomedicina y Genética Molecular (IBGM) de Valladolid, Universidad de Valladolid and Consejo Superior de Investigaciones Científicas (CSIC), IBGM, c/ Sanz y Forés 3, 47003 Valladolid, Spain
Interests: calcium signaling; calcium remodeling in cancer; calcium remodeling in aging and Alzheimer's disease; store-operated calcium entry
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Dr. Sendoa Tajada

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Instituto de Biomedicina y Genética Molecular (IBGM) de Valladolid, Universidad de Valladolid and Consejo Superior de Investigaciones Científicas (CSIC), IBGM, c/ Sanz y Forés 3, 47003 Valladolid, Spain
Interests: cardiovascular physiology; neuroscience; ion channels; calcium signaling; cancer and neurodegeneration

Special Issue Information

Dear Colleagues,

The last few years have seen huge development in the field of calcium signaling, from the improvement of calcium probes that are now tailored and targeted to monitor subcellular calcium changes at almost any resolution to the development of modern technologies for calcium imaging or the identification of critically important molecular players involved in calcium transport and homeostasis. These new tools are allowing the discovery of new insights regarding calcium signaling and most importantly how changes in calcium signaling may contribute to the development of a number of diseases. For instance, the discovery of the molecular machinery involved in store-operated Ca²⁺ entry, the release of Ca²⁺ from intracellular stores at the ER and its modulation by BCl2, or Ca²⁺ transfer from the ER to mitochondria via the mitochondrial Ca²⁺ uniporter may contribute to different pathological situations such as cancer, defective immune responses, and neurodegenerative diseases, among many others. The involvement of calcium dishomeostasis in many different pathological situations is under intense scrutiny in laboratories around the world. The development of new applications for established modulators of calcium fluxes and the de novo synthesis of new drugs may help to accelerate new treatments for old diseases. The present issue is intended to showcase the state of the art of calcium signaling in health and disease with the aim of promoting even further research into calcium for unmet disease diagnostics, prognosis, or treatment.

Dr. Carlos Villalobos
Dr. Sendoa Tajada
Guest Editors

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Keywords

store-operated calcium entry in health and disease
mitochondrial calcium in health and disease
subcellular calcium homeostasis
calcium signaling in cancer
calcium signaling in aging and neurodegenerative disorders
calcium signaling in inflammation and immune response

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Published Papers (4 papers)

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Research

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25 pages, 2250 KiB

Open AccessArticle

SERCA Modulators Reveal Distinct Signaling and Functional Roles of T Lymphocyte Ca²⁺ Stores

by Md Nasim Uddin and David W. Thomas

Int. J. Mol. Sci. 2024, 25(22), 12095; https://doi.org/10.3390/ijms252212095 - 11 Nov 2024

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Abstract

The allosteric SERCA (Sarcoplasmic/Endoplasmic Reticulum Ca²⁺-ATPase) activator CDN1163 has been recently added to the group of pharmacological tools for probing SERCA function. We chose to investigate the effects of the compound on T lymphocyte Ca²⁺ stores, using the well-described Jurkat T lymphocyte as a reliable cell system for Ca²⁺ signaling pathways. Our study identified the lowest concentrations of the SERCA inhibitors thapsigargin (TG) and 2,5-di-(tert butyl)-1,4-benzohydroquinone (tBHQ) capable of releasing Ca²⁺, permitting the differentiation of the TG-sensitive SERCA 2b Ca²⁺ store from the tBHQ-sensitive SERCA 3 Ca²⁺ store. We proceeded to test the effects of CDN1163 on Ca²⁺ stores, examining specific actions on the SERCA 2b and SERCA 3 Ca²⁺ pools using our low-dose SERCA blocker regimen. In contrast to previous work, we find CDN1163 exerts complex time-sensitive and SERCA isoform-specific actions on Ca²⁺ stores. Surprisingly, short-term exposure (0–30 min) to CDN1163 perturbs T cell Ca²⁺ stores by suppressing Ca²⁺ uptake with diminished Ca²⁺ release from the SERCA 2b-controlled store. Concomitantly, we find evidence for a SERCA-activating effect of CDN1163 on the SERCA-3 regulated store, given the observation of increased Ca²⁺ release inducible by low-dose tBHQ. Intriguingly, longer-term (>12 h) CDN1163 exposure reversed this pattern, with increased Ca²⁺ release from SERCA 2b-regulated pools yet decreased Ca²⁺ release responses from the tBHQ-sensitive SERCA 3 pool. Indeed, this remodeling of SERCA 2b Ca²⁺ stores with longer-term CDN1163 exposure also translated into the compound’s ability to protect Jurkat T lymphocytes from TG but not tBHQ-induced growth suppression. Full article

(This article belongs to the Special Issue Calcium Signaling in Health and Diseases)

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18 pages, 3495 KiB

Open AccessArticle

SARS-CoV-2 Viroporin E Induces Ca²⁺ Release and Neuron Cell Death in Primary Cultures of Rat Hippocampal Cells Aged In Vitro

by Sara López-Vázquez, Carlos Villalobos and Lucía Núñez

Int. J. Mol. Sci. 2024, 25(12), 6304; https://doi.org/10.3390/ijms25126304 - 7 Jun 2024

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Abstract

The COVID-19 pandemic was caused by infection with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), which may lead to serious respiratory, vascular and neurological dysfunctions. The SARS-CoV-2 envelope protein (E protein) is a structural viroporin able to form ion channels in cell membranes, which is critical for viral replication. However, its effects in primary neurons have not been addressed. Here we used fluorescence microscopy and calcium imaging to study SARS-CoV-2 viroporin E localization and the effects on neuron damage and intracellular Ca²⁺ homeostasis in a model of rat hippocampal neurons aged in vitro. We found that the E protein quickly enters hippocampal neurons and colocalizes with the endoplasmic reticulum (ER) in both short-term (6–8 days in vitro, DIV) and long-term (20–22 DIV) cultures resembling young and aged neurons, respectively. Strikingly, E protein treatment induces apoptosis in aged neurons but not in young neurons. The E protein induces variable increases in cytosolic Ca²⁺ concentration in hippocampal neurons. Ca²⁺ responses to the E protein are due to Ca²⁺ release from intracellular stores at the ER. Moreover, E protein-induced Ca²⁺ release is very small in young neurons and increases dramatically in aged neurons, consistent with the enhanced Ca²⁺ store content in aged neurons. We conclude that the SARS-CoV-2 E protein quickly translocates to ER endomembranes of rat hippocampal neurons where it releases Ca²⁺, probably acting like a viroporin, thus producing Ca²⁺ store depletion and neuron apoptosis in aged neurons and likely contributing to neurological damage in COVID-19 patients. Full article

(This article belongs to the Special Issue Calcium Signaling in Health and Diseases)

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17 pages, 3563 KiB

Open AccessArticle

Unravelling the Collective Calcium Dynamics of Physiologically Aged Astrocytes under a Hypoxic State In Vitro

by Elena V. Mitroshina, Mikhail I. Krivonosov, Alexander M. Pakhomov, Laysan E. Yarullina, Maria S. Gavrish, Tatiana A. Mishchenko, Roman S. Yarkov and Maria V. Vedunova

Int. J. Mol. Sci. 2023, 24(15), 12286; https://doi.org/10.3390/ijms241512286 - 31 Jul 2023

Cited by 2 | Viewed by 1860

Abstract

Astrocytes serve many functions in the brain related to maintaining nerve tissue homeostasis and regulating neuronal function, including synaptic transmission. It is assumed that astrocytes are crucial players in determining the physiological or pathological outcome of the brain aging process and the development of neurodegenerative diseases. Therefore, studies on the peculiarities of astrocyte physiology and interastrocytic signaling during aging are of utmost importance. Calcium waves are one of the main mechanisms of signal transmission between astrocytes, and in the present study we investigated the features of calcium dynamics in primary cultures of murine cortical astrocytes in physiological aging and hypoxia modeling in vitro. Specifically, we focused on the assessment of calcium network dynamics and the restructuring of the functional network architecture in primary astrocytic cultures. Calcium imaging was performed on days 21 (“young” astrocyte group) and 150 (“old” astrocyte group) of cultures’ development in vitro. While the number of active cells and frequency of calcium events were decreased, we observed a reduced degree of correlation in calcium dynamics between neighboring cells, which was accompanied by a reduced number of functionally connected cells with fewer and slower signaling events. At the same time, an increase in the mRNA expression of anti-apoptotic factor Bcl-2 and connexin 43 was observed in “old” astrocytic cultures, which can be considered as a compensatory response of cells with a decreased level of intercellular communication. A hypoxic episode aggravates the depression of the connectivity of calcium dynamics of “young” astrocytes rather than that of “old” ones. Full article

(This article belongs to the Special Issue Calcium Signaling in Health and Diseases)

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Review

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17 pages, 2260 KiB

Open AccessReview

Similarities and Differences between the Orai1 Variants: Orai1α and Orai1β

by Isaac Jardin, Alejandro Berna-Erro, Joel Nieto-Felipe, Alvaro Macias, Jose Sanchez-Collado, Jose J. Lopez, Gines M. Salido and Juan A. Rosado

Int. J. Mol. Sci. 2022, 23(23), 14568; https://doi.org/10.3390/ijms232314568 - 23 Nov 2022

Cited by 6 | Viewed by 2427

Abstract

Orai1, the first identified member of the Orai protein family, is ubiquitously expressed in the animal kingdom. Orai1 was initially characterized as the channel responsible for the store-operated calcium entry (SOCE), a major mechanism that allows cytosolic calcium concentration increments upon receptor-mediated IP₃ generation, which results in intracellular Ca²⁺ store depletion. Furthermore, current evidence supports that abnormal Orai1 expression or function underlies several disorders. Orai1 is, together with STIM1, the key element of SOCE, conducting the Ca²⁺ release-activated Ca²⁺ (CRAC) current and, in association with TRPC1, the store-operated Ca²⁺ (SOC) current. Additionally, Orai1 is involved in non-capacitative pathways, as the arachidonate-regulated or LTC4-regulated Ca²⁺ channel (ARC/LRC), store-independent Ca²⁺ influx activated by the secretory pathway Ca²⁺-ATPase (SPCA2) and the small conductance Ca²⁺-activated K⁺ channel 3 (SK3). Furthermore, Orai1 possesses two variants, Orai1α and Orai1β, the latter lacking 63 amino acids in the N-terminus as compared to the full-length Orai1α form, which confers distinct features to each variant. Here, we review the current knowledge about the differences between Orai1α and Orai1β, the implications of the Ca²⁺ signals triggered by each variant, and their downstream modulatory effect within the cell. Full article

(This article belongs to the Special Issue Calcium Signaling in Health and Diseases)

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