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Calcium Signaling in Health and Diseases
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Calcium Signaling in Health and Diseases

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: 20 October 2024 | Viewed by 8295

Special Issue Editors

Dr. Carlos Villalobos

E-Mail Website
Guest Editor
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
Special Issues, Collections and Topics in MDPI journals
Dr. Sendoa Tajada

E-Mail Website
Guest Editor
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

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.

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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 (3 papers)

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Research

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18 pages, 3495 KiB  
Article
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
Viewed by 3347
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, [...] Read more.
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  
Article
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 1775
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 [...] Read more.
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  
Review
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 2296
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 IP [...] Read more.
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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