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Oxygen mediated ion channels

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https://www.readbyqxmd.com/read/28545724/the-role-of-ca-2-in-cell-death-caused-by-oxidative-glutamate-toxicity-and-ferroptosis
#1
REVIEW
Pamela Maher, Klaus van Leyen, Partha Narayan Dey, Birgit Honrath, Amalia Dolga, Axel Methner
Ca(2+) ions play a fundamental role in cell death mediated by oxidative glutamate toxicity or oxytosis, a form of programmed cell death similar and possibly identical to other forms of cell death like ferroptosis. Ca(2+) influx from the extracellular space occurs late in a cascade characterized by depletion of the intracellular antioxidant glutathione, increases in cytosolic reactive oxygen species and mitochondrial dysfunction. Here, we aim to compare oxidative glutamate toxicity with ferroptosis, address the signaling pathways that culminate in Ca(2+) influx and cell death and discuss the proteins that mediate this...
May 12, 2017: Cell Calcium
https://www.readbyqxmd.com/read/28458673/inflammatory-responses-regulating-alveolar-ion-transport-during-pulmonary-infections
#2
REVIEW
Christin Peteranderl, Jacob I Sznajder, Susanne Herold, Emilia Lecuona
The respiratory epithelium is lined by a tightly balanced fluid layer that allows normal O2 and CO2 exchange and maintains surface tension and host defense. To maintain alveolar fluid homeostasis, both the integrity of the alveolar-capillary barrier and the expression of epithelial ion channels and pumps are necessary to establish a vectorial ion gradient. However, during pulmonary infection, auto- and/or paracrine-acting mediators induce pathophysiological changes of the alveolar-capillary barrier, altered expression of epithelial Na,K-ATPase and of epithelial ion channels including epithelial sodium channel and cystic fibrosis membrane conductance regulator, leading to the accumulation of edema and impaired alveolar fluid clearance...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28399409/direct-pharmacological-targeting-of-a-mitochondrial-ion-channel-selectively-kills-tumor-cells-in%C3%A2-vivo
#3
Luigi Leanza, Matteo Romio, Katrin Anne Becker, Michele Azzolini, Livio Trentin, Antonella Managò, Elisa Venturini, Angela Zaccagnino, Andrea Mattarei, Luca Carraretto, Andrea Urbani, Stephanie Kadow, Lucia Biasutto, Veronica Martini, Filippo Severin, Roberta Peruzzo, Valentina Trimarco, Jan-Hendrik Egberts, Charlotte Hauser, Andrea Visentin, Gianpietro Semenzato, Holger Kalthoff, Mario Zoratti, Erich Gulbins, Cristina Paradisi, Ildiko Szabo
The potassium channel Kv1.3 is highly expressed in the mitochondria of various cancerous cells. Here we show that direct inhibition of Kv1.3 using two mitochondria-targeted inhibitors alters mitochondrial function and leads to reactive oxygen species (ROS)-mediated death of even chemoresistant cells independently of p53 status. These inhibitors killed 98% of ex vivo primary chronic B-lymphocytic leukemia tumor cells while sparing healthy B cells. In orthotopic mouse models of melanoma and pancreatic ductal adenocarcinoma, the compounds reduced tumor size by more than 90% and 60%, respectively, while sparing immune and cardiac functions...
April 10, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28370799/through-modulation-of-cardiac-ca-2-handling-ucp2-affects-cardiac-electrophysiology-and-influences-the-susceptibility-for-ca-2-mediated-arrhythmias
#4
Robert Larbig, Sara Reda, Vera Paar, Andrea Trost, Johannes Leitner, Stephanie Weichselbaumer, Karolina A Motloch, Bernhard Wernly, Andreas Arrer, Benjamin Strauss, Michael Lichtenauer, Herbert A Reitsamer, Lars Eckardt, Guiscard Seebohm, Uta C Hoppe, Lukas J Motloch
Introduction UCP2 belongs to a superfamily of mitochondrial ion transporters. Due to its beneficial influence on production of reactive oxygen species it is suggested to reduce cardiac ischemic reperfusion injury. Recent studies uncovered its ability to regulate mitochondrial Ca(2+) -uptake and therefore to influence cardiac cytosolic Ca(2+) -handling, indicating compensatory pathways to avoid toxic Ca(2+) -overload in UCP2 knock-out mice (UCP2(-/-) ). However, the specific mechanisms and their impact on cardiac electrophysiology remain speculative...
March 31, 2017: Experimental Physiology
https://www.readbyqxmd.com/read/28360106/ca-2-and-calpain-mediate-capsaicin-induced-ablation-of-axonal-terminals-expressing-transient-receptor-potential-vanilloid-1
#5
Sheng Wang, Sen Wang, Jamila Asgar, John Joseph, Jin Y Ro, Feng Wei, James N Campbell, Man-Kyo Chung
Capsaicin is an ingredient in spicy peppers that produces burning pain by activating transient receptor potential vanilloid 1 (TRPV1), a Ca(2+)-permeable ion channel in nociceptors. Capsaicin has also been used as an analgesic, and its topical administration is approved for the treatment of certain pain conditions. The mechanisms underlying capsaicin-induced analgesia likely involve reversible ablation of nociceptor terminals. However, the mechanisms underlying these effects are not well understood. To visualize TRPV1-lineage axons, a genetically engineered mouse model was used in which a fluorophore is expressed under the TRPV1 promoter...
May 19, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28351840/macrophages-utilize-the-mitochondrial-calcium-uniporter-for-profibrotic-polarization
#6
Linlin Gu, Jennifer L Larson-Casey, A Brent Carter
Fibrosis in multiple organs, including the liver, kidney, and lung, often occurs secondary to environmental exposure. Asbestos exposure is one important environmental cause of lung fibrosis. The mechanisms that mediate fibrosis is not fully understood, although mitochondrial oxidative stress in alveolar macrophages is critical for fibrosis development. Mitochondrial Ca(2+) levels can be associated with production of reactive oxygen species. Here, we show that patients with asbestosis have higher levels of mitochondrial Ca(2+) compared with normal patients...
March 28, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28300265/catalytic-routes-to-fuels-from-c1-and-oxygenate-molecules
#7
Shuai Wang, Iker Agirrezabal-Telleria, Aditya Bhan, Dante Simonetti, Kazuhiro Takanabe, Enrique Iglesia
This account illustrates concepts in chemical kinetics underpinned by the formalism of transition state theory using catalytic processes that enable the synthesis of molecules suitable as fuels from C1 and oxygenate reactants. Such feedstocks provide an essential bridge towards a carbon-free energy future, but their volatility and low energy density require the formation of new C-C bonds and the removal of oxygen. These transformations are described here through recent advances in our understanding of the mechanisms and site requirements in catalysis by surfaces, with emphasis on enabling concepts that tackle ubiquitous reactivity and selectivity challenges...
April 28, 2017: Faraday Discussions
https://www.readbyqxmd.com/read/28274920/h2o2-augments-cytosolic-calcium-in-nucleus-tractus-solitarii-neurons-via-multiple-voltage-gated-calcium-channels
#8
Tim D Ostrowski, Heather A Dantzler, Luis Polo-Parada, David D Kline
Reactive oxygen species (ROS) play a profound role in cardiorespiratory function under normal physiological conditions and disease states. ROS can influence neuronal activity by altering various ion channels and transporters. Within the nucleus tractus solitarii (nTS), a vital brainstem area for cardiorespiratory control, hydrogen peroxide (H2O2) induces sustained hyperexcitability following an initial depression of neuronal activity. The mechanism(s) associated with the delayed hyperexcitability are unknown...
March 8, 2017: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/28188926/redox-modification-of-caveolar-proteins-in-the-cardiovascular-system-role-in-cellular-signalling-and-disease
#9
REVIEW
Kristen J Bubb, Asa Birna Birgisdottir, Owen Tang, Thomas Hansen, Gemma A Figtree
Rapid and coordinated release of a variety of reactive oxygen species (ROS) such as superoxide (O2(.-)), hydrogen peroxide (H2O2) and peroxynitrite, in specific microdomains, play a crucial role in cell signalling in the cardiovascular system. These reactions are mediated by reversible and functional modifications of a wide variety of key proteins. Dysregulation of this oxidative signalling occurs in almost all forms of cardiovascular disease (CVD), including at the very early phases. Despite the heavily publicized failure of "antioxidants" to improve CVD progression, pharmacotherapies such as those targeting the renin-angiotensin system, or statins, exert at least part of their large clinical benefit via modulating cellular redox signalling...
February 7, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28154371/oxidative-stress-and-calcium-dysregulation-by-palmitate-in-type-2-diabetes
#10
REVIEW
Luong Dai Ly, Shanhua Xu, Seong-Kyung Choi, Chae-Myeong Ha, Themis Thoudam, Seung-Kuy Cha, Andreas Wiederkehr, Claes B Wollheim, In-Kyu Lee, Kyu-Sang Park
Free fatty acids (FFAs) are important substrates for mitochondrial oxidative metabolism and ATP synthesis but also cause serious stress to various tissues, contributing to the development of metabolic diseases. CD36 is a major mediator of cellular FFA uptake. Inside the cell, saturated FFAs are able to induce the production of cytosolic and mitochondrial reactive oxygen species (ROS), which can be prevented by co-exposure to unsaturated FFAs. There are close connections between oxidative stress and organellar Ca(2+) homeostasis...
February 3, 2017: Experimental & Molecular Medicine
https://www.readbyqxmd.com/read/28117962/acidotoxicity-via-asic1a-mediates-cell-death-during-oxygen-glucose-deprivation-and-abolishes-excitotoxicity
#11
Saurav Bhowmick, Jeanette T Moore, Daniel L Kirschner, Mary C Curry, Emily G Westbrook, Brian T Rasley, Kelly L Drew
Ischemic reperfusion (I/R) injury is associated with a complex and multifactorial cascade of events involving excitotoxicity, acidotoxicity, and ionic imbalance. While it is known that acidosis occurs concomitantly with glutamate-mediated excitotoxicity during brain ischemia, it remains elusive how acidosis-mediated acidotoxicity interacts with glutamate-mediated excitotoxicity. Here, we investigated the effect of acidosis on glutamate-mediated excitotoxicity in acute hippocampal slices. We tested the hypothesis that mild acidosis protects against I/R injury via modulation of NMDAR, but produces injury via activation of acid sensing ion channels (ASIC1a)...
March 1, 2017: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/28004868/physiological-redox-signalling-and-regulation-of-ion-channels-implications-for-pulmonary-hypertension
#12
Jeremy P T Ward
Pulmonary hypertension is associated with oxidant stress and increased generation of reactive oxygen species (ROS) by NADPH oxidases (NOX), mitochondria and other sources. There is considerable evidence that these contribute to the aetiology via promotion of pulmonary vascular remodelling, endothelial dysfunction and enhanced vasoreactivity. However, it is now recognised that ROS act as important signalling mediators and second messengers under normal physiological conditions. Many ion channels and protein kinases critical to pulmonary vascular function are directly or indirectly affected by redox/ROS, including K(+) , Ca(2+) and nonselective cation channels and Rho kinase...
December 22, 2016: Experimental Physiology
https://www.readbyqxmd.com/read/27957685/trpm2-promotes-neurotoxin-mpp-mptp-induced-cell-death
#13
Yuyang Sun, Pramod Sukumaran, Senthil Selvaraj, Nicholas I Cilz, Anne Schaar, Saobo Lei, Brij B Singh
In neurons, Ca(2+) is essential for a variety of physiological processes that regulate gene transcription to neuronal growth and their survival. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridinium ions (MPP(+)) are potent neurotoxins that selectively destroys the dopaminergic (DA) neurons and mimics Parkinson's disease (PD) like symptoms, but the mechanism as how MPP(+)/MPTP effects DA neuron survival is not well-understood. In the present study, we found that MPP(+) treatment increased the level of reactive oxygen species (ROS) that activates and upregulates the expression and function of melastatin-like transient receptor potential (TRPM) subfamily member, melastatin-like transient receptor potential channel 2 (TRPM2)...
December 12, 2016: Molecular Neurobiology
https://www.readbyqxmd.com/read/27941930/erk-mediated-nf-%C3%AE%C2%BAb-activation-through-asic1-in-response-to-acidosis
#14
B Chen, J Liu, T-T Ho, X Ding, Y-Y Mo
Acidic microenvironment is a common feature of solid tumors. We have previously shown that neuron specific acid-sensing ion channel 1 (ASIC1) is expressed in breast cancer, and it is responsible for acidosis-induced cellular signaling through AKT, leading to nuclear factor-κB (NF-κB) activation, and cell invasion and metastasis. However, AKT is frequently activated in cancer. Thus, a key question is whether ASIC1-mediated cell signaling still takes place in the cancer cells carrying constitutively active AKT...
December 12, 2016: Oncogenesis
https://www.readbyqxmd.com/read/27881662/the-polycystins-are-modulated-by-cellular-oxygen-sensing-pathways-and-regulate-mitochondrial-function
#15
Valeria Padovano, Ivana Y Kuo, Lindsey K Stavola, Hans R Aerni, Benjamin J Flaherty, Hannah C Chapin, Ming Ma, Stefan Somlo, Alessandra Boletta, Barbara E Ehrlich, Jesse Rinehart, Michael J Caplan
Autosomal dominant polycystic kidney disease is caused by mutations in the genes encoding polycystin-1 (PC1) and polycystin-2 (PC2), which form an ion channel complex that may mediate ciliary sensory processes and regulate endoplasmic reticulum (ER) Ca(2+) release. Loss of PC1 expression profoundly alters cellular energy metabolism. The mechanisms that control the trafficking of PC1 and PC2, as well as their broader physiological roles, are poorly understood. We found that O2 levels regulate the subcellular localization and channel activity of the polycystin complex through its interaction with the O2-sensing prolyl hydroxylase domain containing protein EGLN3 (or PHD3), which hydroxylates PC1...
January 15, 2017: Molecular Biology of the Cell
https://www.readbyqxmd.com/read/27694440/depletion-of-the-human-ion-channel-trpm2-in-neuroblastoma-demonstrates-its-key-role-in-cell-survival-through-modulation-of-mitochondrial-reactive-oxygen-species-and-bioenergetics
#16
Lei Bao, Shu-Jen Chen, Kathleen Conrad, Kerry Keefer, Thomas Abraham, John P Lee, JuFang Wang, Xue-Qian Zhang, Iwona Hirschler-Laszkiewicz, Hong-Gang Wang, Sinisa Dovat, Brian Gans, Muniswamy Madesh, Joseph Y Cheung, Barbara A Miller
Transient receptor potential melastatin 2 (TRPM2) ion channel has an essential function in modulating cell survival following oxidant injury and is highly expressed in many cancers including neuroblastoma. Here, in xenografts generated from neuroblastoma cells in which TRPM2 was depleted with CRISPR/Cas9 technology and in in vitro experiments, tumor growth was significantly inhibited and doxorubicin sensitivity increased. The hypoxia-inducible transcription factor 1/2α (HIF-1/2α) signaling cascade including proteins involved in oxidant stress, glycolysis, and mitochondrial function was suppressed by TRPM2 depletion...
November 18, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27625993/news-about-vdac1-in-hypoxia
#17
N M Mazure
The voltage-dependent anion channel (VDAC) is the main interface between the cytosol and mitochondria of cells. It plays a crucial role in both mitochondrial metabolism and cell death. The main basic function of this channel is to mediate and gate the flux of small ions, metabolites, and adenosine triphosphate. Changes in its structure, and thus conformation, are expected to affect its activity and modulate the ability of cancer cells to expand. In this review, we describe a novel mechanism by which mitochondria of cells in hypoxia, a low level of oxygen, protects from apoptosis...
2016: Frontiers in Oncology
https://www.readbyqxmd.com/read/27563092/a-15-step-synthesis-of-ryanodol
#18
Kangway V Chuang, Chen Xu, Sarah E Reisman
(+)-Ryanodine and (+)-ryanodol are complex diterpenoids that modulate intracellular calcium-ion release at ryanodine receptors, ion channels critical for skeletal and cardiac muscle excitation-contraction coupling and synaptic transmission. Chemical derivatization of these diterpenoids has demonstrated that certain peripheral structural modifications can alter binding affinity and selectivity among ryanodine receptor isoforms. Here, we report a short chemical synthesis of (+)-ryanodol that proceeds in only 15 steps from the commercially available terpene (S)-pulegone...
August 26, 2016: Science
https://www.readbyqxmd.com/read/27559140/a-neuronal-lactate-uptake-inhibitor-slows-recovery-of-extracellular-ion-concentration-changes-in-the-hippocampal-ca3-region-by-affecting-energy-metabolism
#19
Eskedar Ayele Angamo, Joerg Rösner, Agustin Liotta, Richard Kovács, Uwe Heinemann
Astrocyte-derived lactate supports pathologically enhanced neuronal metabolism, but its role under physiological conditions is still a matter of debate. Here, we determined the contribution of astrocytic neuronal lactate shuttle for maintenance of ion homeostasis and energy metabolism. We tested for the effects of α-cyano-4-hydroxycinnamic acid (4-CIN), which could interfere with energy metabolism by blocking monocarboxylate-transporter 2 (MCT2)-mediated neuronal lactate uptake, on evoked potentials, stimulus-induced changes in K(+), Na(+), Ca(2+), and oxygen concentrations as well as on changes in flavin adenine dinucleotide (FAD) autofluorescence in the hippocampal area CA3...
November 1, 2016: Journal of Neurophysiology
https://www.readbyqxmd.com/read/27494181/identification-of-kca3-1-channel-as-a-novel-regulator-of-oxidative-phosphorylation-in-a-subset-of-pancreatic-carcinoma-cell-lines
#20
Ilya Kovalenko, Andrea Glasauer, Laura Schöckel, Daniel R P Sauter, Alexander Ehrmann, Florian Sohler, Andrea Hägebarth, Ivana Novak, Sven Christian
Pancreatic ductal adenocarcinoma (PDAC) represents the most common form of pancreatic cancer with rising incidence in developing countries and overall 5-year survival rates of less than 5%. The most frequent mutations in PDAC are gain-of-function mutations in KRAS as well as loss-of-function mutations in p53. Both mutations have severe impacts on the metabolism of tumor cells. Many of these metabolic changes are mediated by transporters or channels that regulate the exchange of metabolites and ions between the intracellular compartment and the tumor microenvironment...
2016: PloS One
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