Special Issue "Organellar Calcium Signaling in Physiology and Pathophysiology"

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

Deadline for manuscript submissions: 15 December 2019.

Special Issue Editors

Prof. Dr. Mohamed Trebak
E-Mail Website
Guest Editor
Department of Cellular and Molecular Physiology, The Pennsylvania State University, Hershey, PA 17033, USA
Interests: STIM/Orai Ca2+ channels; Transient Receptor Potential (TRP) cation channels
Dr. Yassine El Hiani
E-Mail Website
Guest Editor
Department of Physiology and Biophysics, Dalhousie University, Halifax, NS B3H4R2, Canada
Interests: The potential link between TRp channels and oxidative stress signaling in cancer and diabetes

Special Issue Information

Dear Colleagues,

Organellar function exists as a tightly regulated network of signalling cascades, each modulating different aspects of cellular physiology, from ATP synthesis to anti-oxidant defence systems and cell death. The function of these organelles is also influenced by the membrane composition and the structural organization and distribution of each organelle within the cell. However, despite the differences in the above-mentioned characteristics, organelles’ mode of action appears similar when they act as Ca2+-buffer and Ca2+-sensor factories. In response to various stimuli, organelles modulate Ca2+ signalling directly by importing Ca2+ via specific proteins embedded in the organellar membranes, or indirectly through the release of metabolites and messengers that can activate the Ca2+ signalling machinery. This intimate relationship between organelles and Ca2+ signalling lays the foundation for cellular decision-making, ultimately influencing cell survival. Therefore, given their importance in maintaining cellular homeostasis, any disturbance in the function of an organelle often results in the development of severe diseases, many of which have yet to be fully understood.

The aim of this Special Issue is to provide an overview summarizing our current knowledge regarding the underlying molecular mechanisms of organellar Ca2+ signalling in the context of normal cell physiology as well as disease, with special focus on the endoplasmic reticulum, lysosomes, and mitochondria.

Prof. Dr. Mohamed Trebak
Dr. Yassine El Hiani
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 papers will be 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 monthly 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 1800 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

  • organellar Ca2+
  • endoplasmic reticulum
  • lysosomes
  • mitochondria
  • peroxisomes

Published Papers (3 papers)

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Research

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Open AccessArticle
Photosensitizer Activation Drives Apoptosis by Interorganellar Ca2+ Transfer and Superoxide Production in Bystander Cancer Cells
Cells 2019, 8(10), 1175; https://doi.org/10.3390/cells8101175 - 29 Sep 2019
Abstract
In cells, photosensitizer (PS) activation by visible light irradiation triggers reactive oxygen species (ROS) formation, followed by a cascade of cellular responses involving calcium (Ca2+) and other second messengers, resulting in cell demise. Cytotoxic effects spread to nearby cells not exposed [...] Read more.
In cells, photosensitizer (PS) activation by visible light irradiation triggers reactive oxygen species (ROS) formation, followed by a cascade of cellular responses involving calcium (Ca2+) and other second messengers, resulting in cell demise. Cytotoxic effects spread to nearby cells not exposed to light by poorly characterized so-called “bystander effects”. To elucidate the mechanisms involved in bystander cell death, we used both genetically encoded biosensors and fluorescent dyes. In particular, we monitored the kinetics of interorganellar Ca2+ transfer and the production of mitochondrial superoxide anion (O2) and hydrogen peroxide (H2O2) in irradiated and bystander B16-F10 mouse melanoma cancer cells. We determined that focal PS photoactivation in a single cell triggers Ca2+ release from the endoplasmic reticulum (ER) also in the surrounding nonexposed cells, paralleled by mitochondrial Ca2+ uptake. Efficient Ca2+ efflux from the ER was required to promote mitochondrial O2 production in these bystander cells. Our results support a key role for ER–mitochondria communication in the induction of ROS-mediated apoptosis in both direct and indirect photodynamical cancer cell killing. Full article
(This article belongs to the Special Issue Organellar Calcium Signaling in Physiology and Pathophysiology)
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Review

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Open AccessReview
Roles for the Endoplasmic Reticulum in Regulation of Neuronal Calcium Homeostasis
Cells 2019, 8(10), 1232; https://doi.org/10.3390/cells8101232 - 10 Oct 2019
Abstract
By influencing Ca2+ homeostasis in spatially and architecturally distinct neuronal compartments, the endoplasmic reticulum (ER) illustrates the notion that form and function are intimately related. The contribution of ER to neuronal Ca2+ homeostasis is attributed to the organelle being the largest [...] Read more.
By influencing Ca2+ homeostasis in spatially and architecturally distinct neuronal compartments, the endoplasmic reticulum (ER) illustrates the notion that form and function are intimately related. The contribution of ER to neuronal Ca2+ homeostasis is attributed to the organelle being the largest reservoir of intracellular Ca2+ and having a high density of Ca2+ channels and transporters. As such, ER Ca2+ has incontrovertible roles in the regulation of axodendritic growth and morphology, synaptic vesicle release, and neural activity dependent gene expression, synaptic plasticity, and mitochondrial bioenergetics. Not surprisingly, many neurological diseases arise from ER Ca2+ dyshomeostasis, either directly due to alterations in ER resident proteins, or indirectly via processes that are coupled to the regulators of ER Ca2+ dynamics. In this review, we describe the mechanisms involved in the establishment of ER Ca2+ homeostasis in neurons. We elaborate upon how changes in the spatiotemporal dynamics of Ca2+ exchange between the ER and other organelles sculpt neuronal function and provide examples that demonstrate the involvement of ER Ca2+ dyshomeostasis in a range of neurological and neurodegenerative diseases. Full article
(This article belongs to the Special Issue Organellar Calcium Signaling in Physiology and Pathophysiology)
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Open AccessFeature PaperReview
Calcium Dyshomeostasis and Lysosomal Ca2+ Dysfunction in Amyotrophic Lateral Sclerosis
Cells 2019, 8(10), 1216; https://doi.org/10.3390/cells8101216 - 08 Oct 2019
Abstract
Recent findings in the understanding of amyotrophic lateral sclerosis (ALS) revealed that alteration in calcium (Ca2+) homeostasis may largely contribute to motor neuron demise. A large part of these alterations is due to dysfunctional Ca2+-storing organelles, including the endoplasmic [...] Read more.
Recent findings in the understanding of amyotrophic lateral sclerosis (ALS) revealed that alteration in calcium (Ca2+) homeostasis may largely contribute to motor neuron demise. A large part of these alterations is due to dysfunctional Ca2+-storing organelles, including the endoplasmic reticulum (ER) and mitochondria. Very recently, lysosomal Ca2+ dysfunction has emerged as an important pathological change leading to neuronal loss in ALS. Remarkably, the Ca2+-storing organelles are interacting with each other at specialized domains controlling mitochondrial dynamics, ER/lysosomal function, and autophagy. This occurs as a result of interaction between specific ionic channels and Ca2+-dependent proteins located in each structure. Therefore, the dysregulation of these ionic mechanisms could be considered as a key element in the neurodegenerative process. This review will focus on the possible role of lysosomal Ca2+ dysfunction in the pathogenesis of several neurodegenerative diseases, including ALS and shed light on the possibility that specific lysosomal Ca2+ channels might represent new promising targets for preventing or at least delaying neurodegeneration in ALS. Full article
(This article belongs to the Special Issue Organellar Calcium Signaling in Physiology and Pathophysiology)
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