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      Calcium and ROS: A mutual interplay

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          Abstract

          Calcium is an important second messenger involved in intra- and extracellular signaling cascades and plays an essential role in cell life and death decisions. The Ca 2+ signaling network works in many different ways to regulate cellular processes that function over a wide dynamic range due to the action of buffers, pumps and exchangers on the plasma membrane as well as in internal stores. Calcium signaling pathways interact with other cellular signaling systems such as reactive oxygen species (ROS). Although initially considered to be potentially detrimental byproducts of aerobic metabolism, it is now clear that ROS generated in sub-toxic levels by different intracellular systems act as signaling molecules involved in various cellular processes including growth and cell death. Increasing evidence suggests a mutual interplay between calcium and ROS signaling systems which seems to have important implications for fine tuning cellular signaling networks. However, dysfunction in either of the systems might affect the other system thus potentiating harmful effects which might contribute to the pathogenesis of various disorders.

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          Highlights

          • Calcium and ROS act as signaling molecules inside the cell and their pathways can interact.

          • The mutual interplay of calcium and ROS is required for the fine tuning of signaling.

          • Failure in the interplay results in dysfunction and pathologies.

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          Most cited references140

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          ER stress-induced cell death mechanisms.

          The endoplasmic-reticulum (ER) stress response constitutes a cellular process that is triggered by a variety of conditions that disturb folding of proteins in the ER. Eukaryotic cells have developed an evolutionarily conserved adaptive mechanism, the unfolded protein response (UPR), which aims to clear unfolded proteins and restore ER homeostasis. In cases where ER stress cannot be reversed, cellular functions deteriorate, often leading to cell death. Accumulating evidence implicates ER stress-induced cellular dysfunction and cell death as major contributors to many diseases, making modulators of ER stress pathways potentially attractive targets for therapeutics discovery. Here, we summarize recent advances in understanding the diversity of molecular mechanisms that govern ER stress signaling in health and disease. This article is part of a Special Section entitled: Cell Death Pathways. © 2013.
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            Mitochondria as sensors and regulators of calcium signalling.

            During the past two decades calcium (Ca(2+)) accumulation in energized mitochondria has emerged as a biological process of utmost physiological relevance. Mitochondrial Ca(2+) uptake was shown to control intracellular Ca(2+) signalling, cell metabolism, cell survival and other cell-type specific functions by buffering cytosolic Ca(2+) levels and regulating mitochondrial effectors. Recently, the identity of mitochondrial Ca(2+) transporters has been revealed, opening new perspectives for investigation and molecular intervention.
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              A tissue-scale gradient of hydrogen peroxide mediates rapid wound detection in zebrafish

              Barrier structures (e.g. epithelia around tissues, plasma membranes around cells) are required for internal homeostasis and protection from pathogens. Wound detection and healing represent a dormant morphogenetic program that can be rapidly executed to restore barrier integrity and tissue homeostasis. In animals, initial steps include recruitment of leukocytes to the site of injury across distances of hundreds of micrometers within minutes of wounding. The spatial signals that direct this immediate tissue response are unknown. Due to their fast diffusion and versatile biological activities, reactive oxygen species (ROS), including hydrogen peroxide (H2O2), are interesting candidates for wound-to-leukocyte signalling. We probed the role of H2O2 during the early events of wound responses in zebrafish larvae expressing a genetically encoded H2O2 sensor1. This reporter revealed a sustained rise in H2O2 concentration at the wound margin, starting ∼3 min after wounding and peaking at ∼20 min, which extended ∼100−200 μm into the tail fin epithelium as a decreasing concentration gradient. Using pharmacological and genetic inhibition, we show that this gradient is created by Dual oxidase (Duox), and that it is required for rapid recruitment of leukocytes to the wound. This is the first observation of a tissue-scale H2O2 pattern, and the first evidence that H2O2 signals to leukocytes in tissues, in addition to its known antiseptic role.
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                Author and article information

                Contributors
                Journal
                Redox Biol
                Redox Biol
                Redox Biology
                Elsevier
                2213-2317
                11 August 2015
                December 2015
                11 August 2015
                : 6
                : 260-271
                Affiliations
                [a ]Experimental and Molecular Pediatric Cardiology, German Heart Center Munich at the Technical University Munich, Germany
                [b ]DZHK (German Centre for Cardiovascular Research), Partner Site Munich Heart Alliance, Munich, Germany
                [c ]Center for Molecular Medicine, Slovak Academy of Sciences, Bratislava, Slovakia
                [d ]Institute of Virology, Slovak Academy of Sciences, Bratislava, Slovakia
                Author notes
                [* ]Corresponding author at: Experimental and Molecular Pediatric Cardiology, German Heart Center Munich at the Technical University Munich, Lazarettstr. 36, 80636 Munich, Germany. Fax: +49 8 91281 2633.Experimental and Molecular Pediatric Cardiology, German Heart Center Munich at the Technical University MunichLazarettstr. 36Munich80636Germany goerlach@ 123456dhm.mhn.de
                [** ]Corresponding author at: Center for Molecular Medicine, Slovak Academy of Sciences, Vlarska 7, 831 01 Bratislava, Slovakia. Fax: +421 2 54773666.Center for Molecular Medicine, Slovak Academy of SciencesVlarska 7Bratislava831 01Slovakia olga.krizanova@ 123456savba.sk
                Article
                S2213-2317(15)00100-7 REDOXD1500102
                10.1016/j.redox.2015.08.010
                4556774
                26296072
                3d982000-86a1-4193-9f2b-af9e390590fd
                © 2015 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 1 July 2015
                : 8 August 2015
                : 10 August 2015
                Categories
                Review Article

                calcium,reactive oxygen species,mitochondria,nadph oxidases,endoplasmic reticulum,channels

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