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https://www.readbyqxmd.com/read/28726639/mitochondrial-calcium-uniporter-in-drosophila-transfers-calcium-between-the-endoplasmic-reticulum-and-mitochondria-in-oxidative-stress-induced-cell-death
#1
Sekyu Choi, Xianglan Quan, Sunhoe Bang, Heesuk Yoo, Jiyoung Kim, Jiwon Park, Kyu-Sang Park, Jongkyeong Chung
Mitochondrial calcium plays critical roles in diverse cellular processes ranging from energy metabolism to cell death. Previous studies have demonstrated that mitochondrial calcium uptake is mainly mediated by the mitochondrial calcium uniporter (MCU) complex. However, the roles of the MCU complex in calcium transport, signaling, and dysregulation by oxidative stress still remain unclear. Here, we confirmed that Drosophila MCU contains evolutionarily conserved structures and requires essential MCU regulator (EMRE) for its calcium channel activities...
July 18, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28725634/ip3-receptor-mediated-calcium-signaling-and-its-role-in-autophagy-in-cancer
#2
REVIEW
Elzbieta Kania, Gemma Roest, Tim Vervliet, Jan B Parys, Geert Bultynck
Calcium ions (Ca(2+)) play a complex role in orchestrating diverse cellular processes, including cell death and survival. To trigger signaling cascades, intracellular Ca(2+) is shuffled between the cytoplasm and the major Ca(2+) stores, the endoplasmic reticulum (ER), the mitochondria, and the lysosomes. A key role in the control of Ca(2+) signals is attributed to the inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs), the main Ca(2+)-release channels in the ER. IP3Rs can transfer Ca(2+) to the mitochondria, thereby not only stimulating core metabolic pathways but also increasing apoptosis sensitivity and inhibiting basal autophagy...
2017: Frontiers in Oncology
https://www.readbyqxmd.com/read/28723387/sigma-1-receptor-activation-modifies-intracellular-calcium-exchange-in-the-g93a-hsod1-als-model
#3
Vedrana Tadić, Ayse Malci, Nadine Goldhammer, Beatrice Stubendorff, Saikata Sengupta, Tino Prell, Silke Keiner, Jingyu Liu, Madlen Guenther, Christiane Frahm, Otto W Witte, Julian Grosskreutz
Aberrations in intracellular calcium (Ca(2+)) have been well established within amyotrophic lateral sclerosis (ALS), a severe motor neuron disease. Intracellular Ca(2+) concentration is controlled in part through the endoplasmic reticulum (ER) mitochondria Ca(2+) cycle (ERMCC). The ER supplies Ca(2+) to the mitochondria at close contacts between the two organelles, i.e. the mitochondria-associated ER membranes (MAMs). The Sigma 1 receptor (Sig1R) is enriched at MAMs, where it acts as an inter-organelle signalling modulator...
July 16, 2017: Neuroscience
https://www.readbyqxmd.com/read/28713161/functional-expression-of-the-ca-2-signaling-machinery-in-human-embryonic-stem-cells
#4
Ji-Jun Huang, Yi-Jie Wang, Min Zhang, Peng Zhang, He Liang, Hua-Jun Bai, Xiu-Jian Yu, Huang-Tian Yang
Emerging evidence suggests that Ca(2+) signals are important for the self-renewal and differentiation of human embryonic stem cells (hESCs). However, little is known about the physiological and pharmacological properties of the Ca(2+)-handling machinery in hESCs. In this study we used RT-PCR and Western blotting to analyze the expression profiles of genes encoding Ca(2+)-handling proteins; we also used confocal Ca(2+) imaging and pharmacological approaches to determine the contribution of the Ca(2+)-handling machinery to the regulation of Ca(2+) signaling in hESCs...
July 17, 2017: Acta Pharmacologica Sinica
https://www.readbyqxmd.com/read/28709993/intracellular-calcium-release-through-ip3r-or-ryr-contributes-to-secondary-axonal-degeneration
#5
Ben C Orem, Nicolas Pelisch, Joshua Williams, Jacqueline M Nally, David P Stirling
Severed CNS axons often retract or dieback away from the injury site and fail to regenerate. The precise mechanisms underlying acute axonal dieback and secondary axonal degeneration remain poorly understood. Here we investigate the role of Ca(2+) store mediated intra-axonal Ca(2+) release in acute axonal dieback and secondary axonal degeneration. To differentiate between primary (directly transected) and "bystander" axonal injury (axons spared by the initial injury but then succumb to secondary degeneration) in real-time we use our previously published highly focal laser-induced spinal cord injury (LiSCI) ex vivo model...
July 11, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28696497/role-of-ca2-and-ion-channels-in-the-regulation-of-apoptosis-under-hypoxia
#6
REVIEW
Miaohong Wang, Jin Tan, Yuyang Miao, Mengmeng Li, Qiang Zhang
Hypoxia is a kind of common pathological condition existing in various diseases such as sleep apnea syndrome, myocardial infarction and stroke, which can precipitate the onset of diseases through inducing cell apoptosis. Ca²⁺ is the ubiquitous message in cell. Given the crucial role of Ca2²⁺ in physiology, intracellular Ca²⁺ overload is a significant regulator of apoptosis. Numerous experiments show that hypoxia may cause changes of multiple cellular Ca²⁺ channels, for instance, Na⁺/ Ca²⁺ Exchanger (NCX), L-type voltage dependent Ca²⁺ channel (L-VDCC), inositol triphosphate receptors (IP3R) and so on, which contribute to intracellular Ca²⁺ overload, thus eventually triggering cell apoptosis...
July 11, 2017: Histology and Histopathology
https://www.readbyqxmd.com/read/28676489/voltage-dependent-ca-2-entry-into-smooth-muscle-during-contraction-promotes-endothelium-mediated-feedback-vasodilation-in-arterioles
#7
Christopher J Garland, Pooneh Bagher, Chloe Powell, Xi Ye, Hamish A L Lemmey, Lyudmyla Borysova, Kim A Dora
Vascular smooth muscle contraction is suppressed by feedback dilation mediated by the endothelium. In skeletal muscle arterioles, this feedback can be activated by Ca(2+) signals passing from smooth muscle through gap junctions to endothelial cells, which protrude through holes in the internal elastic lamina to make contact with vascular smooth muscle cells. Although hypothetically either Ca(2+) or inositol trisphosphate (IP3) may provide the intercellular signal, it is generally thought that IP3 diffusion is responsible...
July 4, 2017: Science Signaling
https://www.readbyqxmd.com/read/28669047/melatonin-protected-cardiac-microvascular-endothelial-cells-against-oxidative-stress-injury-via-suppression-of-ip3r-ca-2-c-vdac-ca-2-m-axis-by-activation-of-mapk-erk-signaling-pathway
#8
Hang Zhu, Qinhua Jin, Yang Li, Qiang Ma, Jing Wang, Dandan Li, Hao Zhou, Yundai Chen
The cardiac microvascular reperfusion injury is characterized by the microvascular endothelial cells (CMECs) oxidative damage which is responsible for the progression of cardiac dysfunction. However, few strategies are available to reverse such pathologies. This study aimed to explore the mechanism by which oxidative stress induced CMECs death and the beneficial actions of melatonin on CMECs survival, with a special focused on IP3R-[Ca(2+)]c/VDAC-[Ca(2+)]m damage axis and the MAPK/ERK survival signaling. We found that oxidative stress induced by H2O2 significantly activated cAMP response element binding protein (CREB) that enhanced IP3R and VDAC transcription and expression, leading to [Ca(2+)]c and [Ca(2+)]m overload...
July 1, 2017: Cell Stress & Chaperones
https://www.readbyqxmd.com/read/28667050/regional-heterogeneity-in-the-mechanisms-of-myogenic-tone-in-hamster-arterioles
#9
William F Jackson, Erika M Boerman
Myogenic tone is an important feature of arterioles and resistance arteries, but the mechanisms responsible for this hallmark characteristic remain unclear. We utilized pharmacological inhibitors to compare the roles played by phospholipase C (PLC; 10 μM U73122), inositol 1,4,5 trisphosphate receptors (IP3R; 100 μM 2-Aminoethoxydiphenylborane, 2-APB), protein kinase C (PKC; 10μM Bisindolylmaleimide I), angiotensin II type 1 receptors (AT1R; 1μM losartan), Rho-kinase (10nM-30μM Y27632 or 300nM H1152), stretch-activated ion channels (10nM-1μM Gd(3+) or 5μM spider venom toxin GsMTx-4) and L-type voltage-gated Ca(2+) channels (0...
June 30, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28660247/phototransduction-in-drosophila-is-compromised-by-gal4-expression-but-not-by-insp3-receptor-knockdown-or-mutation
#10
Murali K Bollepalli, Marije E Kuipers, Che-Hsiung Liu, Sabrina Asteriti, Roger C Hardie
Drosophila phototransduction is mediated by phospholipase C, leading to activation of transient receptor potential (TRP) and TRP-like (TRPL) channels by mechanisms that are unresolved. A role for InsP3 receptors (IP3Rs) had been excluded because IP3R mutants (itpr) appeared to have normal light responses; however, this was recently challenged by Kohn et al. ("Functional cooperation between the IP3 receptor and phospholipase C secures the high sensitivity to light of Drosophila photoreceptors in vivo," Journal of Neuroscience 35:2530), who reported defects in phototransduction after IP3R-RNAi knockdown...
May 2017: ENeuro
https://www.readbyqxmd.com/read/28644055/regulation-of-transient-receptor-potential-melastatin-4-channel-by-sarcoplasmic-reticulum-inositol-trisphosphate-receptors-role-in-human-detrusor-smooth-muscle-function
#11
Aaron Provence, Eric S Rovner, Georgi V Petkov
We recently reported key physiologic roles for Ca(2+)-activated transient receptor potential melastatin 4 (TRPM4) channels in detrusor smooth muscle (DSM). However, the Ca(2+)-signaling mechanisms governing TRPM4 channel activity in human DSM cells are unexplored. As the TRPM4 channels are activated by Ca(2+), inositol 1,4,5-trisphosphate receptor (IP3R)-mediated Ca(2+) release from the sarcoplasmic reticulum represents a potential Ca(2+) source for TRPM4 channel activation. We used clinically-characterized human DSM tissues to investigate the molecular and functional interactions of the IP3Rs and TRPM4 channels...
June 23, 2017: Channels
https://www.readbyqxmd.com/read/28642246/modulation-of-endoplasmic-reticulum-stress-controls-cd4-t-cell-activation-and-anti-tumor-function
#12
Jessica E Thaxton, Caroline Wallace, Brian Riesenberg, Yongliang Zhang, Chrystal Paulos, Craig Beeson, Bei Liu, Zihai Li
The endoplasmic reticulum (ER) is an energy-sensing organelle with intimate ties to programming cell activation and metabolic fate. T-cell receptor (TCR) activation represents a form of acute cell stress and induces mobilization of ER Ca(2+) stores. The role of the ER in programming T-cell activation and metabolic fate remains largely undefined. Gp96 is an ER protein with functions as a molecular chaperone and Ca(2+) buffering protein. We hypothesized that the ER stress response may be important for CD4(+) T-cell activation and that gp96 may be integral to this process...
June 22, 2017: Cancer Immunology Research
https://www.readbyqxmd.com/read/28637808/dmt-efficiently-inhibits-hepatic-gluconeogenesis-involving-g%C3%AE-q-signaling-pathway
#13
Ting-Ting Zhou, Fei Ma, Xiao-Fan Shi, Xin Xu, Te Du, Xiao-Dan Guo, Gai-Hong Wang, Liang Yu, Vatcharin Rukachaisirikul, Li-Hong Hu, Jing Chen, Xu Shen
Type 2 diabetes mellitus (T2DM) is a chronic metabolic disease with complicated pathogenesis, and targeting gluconeogenesis inhibition is a promising strategy for anti-diabetic drug discovery. G protein-coupled receptors (GPCRs) are classified as distinct families by heterotrimeric G proteins, primarily including Gαs, Gαi and Gαq. Gαs-coupled GPCRs function potently in the regulation of hepatic gluconeogenesis through activating cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) pathway, and Gαi-coupled GPCRs exhibit inhibitory effect on adenylyl cyclase and reduce intracellular cAMP level...
June 21, 2017: Journal of Molecular Endocrinology
https://www.readbyqxmd.com/read/28629579/role-of-soce-architects-stim-and-orai-proteins-in-cell-death
#14
REVIEW
Jyoti Tanwar, Rajender K Motiani
Calcium (Ca(2+)) signaling plays a critical role in regulating plethora of cellular functions including cell survival, proliferation and migration. The perturbations in cellular Ca(2+) homeostasis can lead to cell death either by activating autophagic pathways or through induction of apoptosis. Endoplasmic reticulum (ER) is the major storehouse of Ca(2+) within cells and a number of physiological agonists mediate ER Ca(2+) release by activating IP3 receptors (IP3R). This decrease in ER Ca(2+) levels is sensed by STIM, which physically interacts and activates plasma membrane Ca(2+) selective Orai channels...
June 9, 2017: Cell Calcium
https://www.readbyqxmd.com/read/28620198/hydrogen-gas-protects-ip3rs-by-reducing-disulfide-bridges-in-human-keratinocytes-under-oxidative-stress
#15
Ching-Ying Wu, Wen-Li Hsu, Ming-Hsien Tsai, Jui-Lin Liang, Jian-He Lu, Chia-Jung Yen, Hsin-Su Yu, Mami Noda, Chi-Yu Lu, Chu-Huang Chen, Shian-Jang Yan, Tohru Yoshioka
Based on the oxidative stress theory, aging derives from the accumulation of oxidized proteins induced by reactive oxygen species (ROS) in the cytoplasm. Hydrogen peroxide (H2O2) elicits ROS that induces skin aging through oxidation of proteins, forming disulfide bridges with cysteine or methionine sulfhydryl groups. Decreased Ca(2+) signaling is observed in aged cells, probably secondary to the formation of disulfide bonds among Ca(2+) signaling-related proteins. Skin aging processes are modeled by treating keratinocytes with H2O2...
June 15, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28618351/structure-of-ip3r-channel-high-resolution-insights-from-cryo-em
#16
REVIEW
Mariah R Baker, Guizhen Fan, Irina I Serysheva
Inositol 1,4,5-trisphosphate receptors (IP3Rs) are ubiquitously expressed intracellular Ca(2+) channels and the major mediators of cellular Ca(2+) signals generated by the release of Ca(2+) ions from intracellular stores in response to a variety of extracellular stimuli. Despite established physiological significance and proven involvements of IP3R channels in many human diseases, detailed structural basis for signal detection by these ion channels and their gating remain obscure. Recently, single particle electron cryomicroscopy (cryo-EM) has yielded a long-awaited near-atomic resolution structure of the entire full-length type 1 IP3R...
June 12, 2017: Current Opinion in Structural Biology
https://www.readbyqxmd.com/read/28615414/loss-of-ip3-receptor-mediated-ca-2-release-in-mouse-b-cells-results-in-abnormal-b-cell-development-and-function
#17
Huayuan Tang, Hong Wang, Qingsong Lin, Feifei Fan, Fei Zhang, Xiaohong Peng, Xi Fang, Jie Liu, Kunfu Ouyang
Intracellular calcium (Ca(2+)) mobilization after engagement of the BCR has been proposed to play an important role in B cell development and function. BCR activation causes an initial Ca(2+) release from the endoplasmic reticulum that is mediated by inositol 1,4,5-trisphosphate receptor (IP3R) and then triggers store-operated Ca(2+) entry once endoplasmic reticulum Ca(2+) store is depleted. Store-operated Ca(2+) entry has been shown to regulate B cell function but is dispensable for B cell development. By contrast, the function of IP3R-mediated Ca(2+) release in B cells remains to be determined...
June 14, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/28614300/pten-counteracts-fbxl2-to-promote-ip3r3-and-ca-2-mediated-apoptosis-limiting-tumour-growth
#18
Shafi Kuchay, Carlotta Giorgi, Daniele Simoneschi, Julia Pagan, Sonia Missiroli, Anita Saraf, Laurence Florens, Michael P Washburn, Ana Collazo-Lorduy, Mireia Castillo-Martin, Carlos Cordon-Cardo, Said M Sebti, Paolo Pinton, Michele Pagano
In response to environmental cues that promote IP3 (inositol 1,4,5-trisphosphate) generation, IP3 receptors (IP3Rs) located on the endoplasmic reticulum allow the 'quasisynaptical' feeding of calcium to the mitochondria to promote oxidative phosphorylation. However, persistent Ca(2+) release results in mitochondrial Ca(2+) overload and consequent apoptosis. Among the three mammalian IP3Rs, IP3R3 appears to be the major player in Ca(2+)-dependent apoptosis. Here we show that the F-box protein FBXL2 (the receptor subunit of one of 69 human SCF (SKP1, CUL1, F-box protein) ubiquitin ligase complexes) binds IP3R3 and targets it for ubiquitin-, p97- and proteasome-mediated degradation to limit Ca(2+) influx into mitochondria...
June 22, 2017: Nature
https://www.readbyqxmd.com/read/28570539/monitoring-er-sr-calcium-release-with-the-targeted-ca2-sensor-catcher
#19
Florence N Reddish, Cassandra L Miller, Rakshya Gorkhali, Jenny J Yang
Intracellular calcium (Ca(2+)) transients evoked by extracellular stimuli initiate a multitude of biological processes in living organisms. At the center of intracellular calcium release are the major intracellular calcium storage organelles, the endoplasmic reticulum (ER) and the more specialized sarcoplasmic reticulum (SR) in muscle cells. The dynamic release of calcium from these organelles is mediated by the ryanodine receptor (RyR) and the inositol 1,4,5-triphosphate receptor (IP3R) with refilling occurring through the sarco/endoplasmic reticulum calcium ATPase (SERCA) pump...
May 19, 2017: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/28546857/chloroquine-inhibits-ca-2-permeable-ion-channels-mediated-ca-2-signaling-in-primary-b-lymphocytes
#20
Yi-Fan Wu, Ping Zhao, Xi Luo, Jin-Chao Xu, Lu Xue, Qi Zhou, Mingrui Xiong, Jinhua Shen, Yong-Bo Peng, Meng-Fei Yu, Weiwei Chen, Liqun Ma, Qing-Hua Liu
BACKGROUND: Chloroquine, a bitter tastant, inhibits Ca(2+) signaling, resulting in suppression of B cell activation; however, the inhibitory mechanism remains unclear. RESULTS: In this study, thapsigargin (TG), but not caffeine, induced sustained intracellular Ca(2+) increases in mouse splenic primary B lymphocytes, which were markedly inhibited by chloroquine. Under Ca(2+)-free conditions, TG elicited transient Ca(2+) increases, which additionally elevated upon the restoration of 2 mM Ca(2+)...
2017: Cell & Bioscience
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