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https://www.readbyqxmd.com/read/27913204/the-selective-bcl-2-inhibitor-venetoclax-a-bh3-mimetic-does-not-dysregulate-intracellular-ca-2-signaling
#1
Tamara Vervloessem, Hristina Ivanova, Tomas Luyten, Jan B Parys, Geert Bultynck
Anti-apoptotic B cell-lymphoma-2 (Bcl-2) proteins are emerging as therapeutic targets in a variety of cancers for precision medicines, like the BH3-mimetic drug venetoclax (ABT-199), which antagonizes the hydrophobic cleft of Bcl-2. However, the impact of venetoclax on intracellular Ca(2+) homeostasis and dynamics in cell systems has not been characterized in detail. Here, we show that venetoclax did not affect Ca(2+)-transport systems from the endoplasmic reticulum (ER) in permeabilized cell systems. Venetoclax (1μM) did neither trigger Ca(2+) release by itself nor affect agonist-induced Ca(2+) release in a variety of intact cell models...
November 29, 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27905509/the-er-stress-regulator-bip-mediates-cadmium-induced-autophagy-and-neuronal-senescence
#2
Tao Wang, Yan Yuan, Hui Zou, Jinlong Yang, Shiwen Zhao, Yonggang Ma, Yi Wang, Jianchun Bian, Xuezhong Liu, Jianhong Gu, Zongping Liu, Jiaqiao Zhu
Autophagy is protective in cadmium (Cd)-induced oxidative damage. Endoplasmic reticulum (ER) stress has been shown to induce autophagy in a process requiring the unfolded protein response signalling pathways. Cd treatment significantly increased senescence in neuronal cells, which was aggravated by 3-MA or silencing of Atg5 and abolished by rapamycin. Cd increased expression of ER stress regulators Bip, chop, eIf2α, and ATF4, and activated autophagy as evidenced by upregulated LC3. Moreover, the ER stress inhibitor mithramycin inhibited the expression of ER stress protein chaperone Bip and blocked autophagic flux...
December 1, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27898307/a-ca-2-chelator-ameliorates-chromium-vi-induced-hepatocyte-l-02-injury-via-down-regulation-of-voltage-dependent-anion-channel-1-vdac1-expression
#3
Xing Yi, Fang Xiao, Xiali Zhong, Yujie Duan, Kaihua Liu, Caigao Zhong
Hexavalent chromium could result in cell malfunctions. Intracellular Ca(2+) ([Ca(2+)]i) content and VDAC1 expression are both important features related to cell survial. This study aimed to explore the mechanism of cell injury induced by Cr(VI) and tentatively offer clues to repairing this cell damage using [Ca(2+)]i and VDAC1. L-02 hepatocytes were treated with Cr(VI)/BAPTA, and the levels of [Ca(2+)]i and cell injury associated with Cr(VI) were determined in addition to the effect of BAPTA. The expression of VDAC1 in Cr(VI)-induced cells was evaluated...
November 18, 2016: Environmental Toxicology and Pharmacology
https://www.readbyqxmd.com/read/27896839/dopamine-elevates-and-lowers-astroglial-ca-2-through-distinct-pathways-depending-on-local-synaptic-circuitry
#4
Alistair Jennings, Olga Tyurikova, Lucie Bard, Kaiyu Zheng, Alexey Semyanov, Christian Henneberger, Dmitri A Rusakov
Whilst astrocytes in culture invariably respond to dopamine with cytosolic Ca(2+) rises, the dopamine sensitivity of astroglia in situ and its physiological roles remain unknown. To minimize effects of experimental manipulations on astroglial physiology, here we monitored Ca(2+) in cells connected via gap junctions to astrocytes loaded whole-cell with cytosolic indicators in area CA1 of acute hippocampal slices. Aiming at high sensitivity of [Ca(2+) ] measurements, we also employed life-time imaging of the Ca(2+) indicator Oregon Green BAPTA-1...
November 29, 2016: Glia
https://www.readbyqxmd.com/read/27891586/celastrol-attenuates-cadmium-induced-neuronal-apoptosis-via-inhibiting-ca-2-camkii-dependent-akt-mtor-pathway
#5
Ruijie Zhang, Yu Zhu, Xiaoqing Dong, Beibei Liu, Nana Zhang, Xiaoxue Wang, Lei Liu, Chong Xu, Shile Huang, Long Chen
Cadmium (Cd), an environmental and industrial pollutant, affects the nervous system and consequential neurodegenerative disorders. Recently we have shown that celastrol prevents Cd-induced neuronal cell death partially by suppressing Akt/mTOR pathway. However, the underlying mechanism remains to be elucidated. Here we show that celastrol attenuated Cd-elevated intracellular free calcium ([Ca(2+) ]i ) level and apoptosis in neuronal cells. Celastrol prevented Cd-induced neuronal apoptosis by inhibiting Akt-mediated mTOR pathway, as inhibition of Akt with Akt inhibitor X or ectopic expression of dominant negative Akt reinforced celastrol's prevention of Cd-induced phosphorylation of S6K1/4E-BP1 and cell apoptosis...
November 27, 2016: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/27873143/regulation-of-rac1-gtpase-activity-by-quinine-through-g-protein-and-bitter-taste-receptor-t2r4
#6
Crystal Sidhu, Appalaraju Jaggupilli, Prashen Chelikani, Rajinder P Bhullar
Rac1 belongs to the Rho family of small GTPases and regulates actin cytoskeleton reorganization. T2R4 is a bitter taste receptor belonging to the G protein-coupled receptor family of proteins. In addition to mediating bitter taste perception from the tongue, T2R4s are found in extra-oral tissues, e.g., nasal epithelium, airways, brain, testis suggesting a much broader physiological function for these receptors. Anti-malarial drug and a bitter tasting compound, quinine, is a known agonist for T2R4, whereas BCML (Nα,Nα-Bis(carboxymethyl)-L-lysine) acts as an inverse agonist...
November 22, 2016: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/27829611/sodium-lauryl-sulfate-stimulates-the-generation-of-reactive-oxygen-species-through-interactions-with-cell-membranes
#7
Taeko Mizutani, Ryota Mori, Misaki Hirayama, Yuki Sagawa, Kenji Shimizu, Yuri Okano, Hitoshi Masaki
Sodium lauryl sulfate (SLS), a representative anionic surfactant, is well-known to induce rough skin following single or multiple topical applications. The mechanism by which SLS induces rough skin is thought to result from the disruption of skin moisture function consisting of NMF and epidermal lipids. However, a recent study demonstrated that topically applied SLS easily penetrates into the living cell layers of the epidermis, which suggests that physiological alterations of keratinocytes might cause the SLS-induced rough skin...
December 1, 2016: Journal of Oleo Science
https://www.readbyqxmd.com/read/27797597/zinc-ions-mediate-gastrin-expression-proliferation-and-migration-downstream-of-the-cholecystokinin-2-receptor
#8
Mike Chang, Lin Xiao, Arthur Shulkes, Graham S Baldwin, Oneel Patel
Gastrin, acting via the cholecystokinin-2 receptor (CCK2R), activates its own promoter in a positive-feed-forward loop that may result in hypergastrinemia. Activity of the gastrin promoter is also stimulated by exogenous Zn(2+) ions. Here, the role of intracellular zinc and calcium signaling in the gastrin positive-feed-forward loop was investigated. Gastrin promoter activity was measured in the human gastric carcinoma cell line AGS-CCK2R and in Jurkat cells transfected with various gastrin promoter-luciferase constructs after treatment with gastrin in the presence and absence of zinc- and calcium-chelating agents...
December 2016: Endocrinology
https://www.readbyqxmd.com/read/27796579/calcium-is-not-required-for-triggering-volume-restoration-in-hypotonically-challenged-a549-epithelial-cells
#9
Olga Ponomarchuk, Francis Boudreault, Sergei N Orlov, Ryszard Grygorczyk
Maintenance of cell volume is a fundamental housekeeping function in eukaryotic cells. Acute cell swelling activates a regulatory volume decrease (RVD) process with poorly defined volume sensing and intermediate signaling mechanisms. Here, we analyzed the putative role of Ca(2+) signaling in RVD in single substrate-adherent human lung epithelial A549 cells. Acute cell swelling was induced by perfusion of the flow-through imaging chamber with 50 % hypotonic solution at a defined fluid turnover rate. Changes in cytosolic Ca(2+) concentration ([Ca(2+)]i) and cell volume were monitored simultaneously with ratiometric Fura-2 fluorescence and 3D reconstruction of stereoscopic single-cell images, respectively...
October 31, 2016: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/27790936/effect-of-protriptyline-on-ca-2-i-and-viability-in-mg63-human-osteosarcoma-cells
#10
Ching-Kai Su, Chiang-Ting Chou, Ko-Long Lin, Wei-Zhe Liang, Jin-Shiung Cheng, Hong-Tai Chang, I-Shu Chen, Ti Lu, Chun-Chi Kuo, Chia-Cheng Yu, Pochuen Shieh, Daih-Huang Kuo, Fu-An Chen, Chung-Ren Jan
Tricyclic antidepressants (TCA) have been clinically prescribed in the auxiliary treatment of cancer patients. Although protriptyline, a type of TCA, was used primarily in the clinical treatment of mood disorders in cancer patients, the effect of protriptyline on physiology in human osteosarcoma is unknown. This study examined the effect of protriptyline on cytosolic free Ca(2+ )concentrations ([Ca(2+)]i) and viability in MG63 human osteosarcoma cells. Protriptyline between 50 and 250 μM evoked [Ca(2+)]i rises concentration-dependently...
October 2016: Toxicology Mechanisms and Methods
https://www.readbyqxmd.com/read/27748951/1-fluoro-2-4-dinitrobenzene-and-its-derivatives-act-as-secretagogues-on-rodent-mast-cells
#11
Yohei Manabe, Marie Yoshimura, Kazuma Sakamaki, Asuka Inoue, Aya Kakinoki, Satoshi Hokari, Mariko Sakanaka, Junken Aoki, Hiroyuki Miyachi, Kazuyuki Furuta, Satoshi Tanaka
Accumulating evidence suggests that activated mast cells are involved in contact hypersensitivity, although the precise mechanisms of their activation are still not completely understood. We investigated the potential of common experimental allergens to induce mast cell activation using murine bone marrow-derived cultured mast cells and rat peritoneal mast cells. Among these allergens, 1-chloro-2,4-dinitrobenzene and 1-fluoro-2,4-dinirobenzene (DNFB) were found to induce degranulation of rat peritoneal mast cells...
October 17, 2016: European Journal of Immunology
https://www.readbyqxmd.com/read/27725190/mechanical-strain-stimulates-vasculogenesis-and-expression-of-angiogenesis-guidance-molecules-of-embryonic-stem-cells-through-elevation-of-intracellular-calcium-reactive-oxygen-species-and-nitric-oxide-generation
#12
Fatemeh Sharifpanah, Sascha Behr, Maria Wartenberg, Heinrich Sauer
OBJECTIVES: Differentiation of embryonic stem (ES) cells may be regulated by mechanical strain. Herein, signaling molecules underlying mechanical stimulation of vasculogenesis and expression of angiogenesis guidance cues were investigated in ES cell-derived embryoid bodies. METHODS AND RESULTS: Treatment of embryoid bodies with 10% static mechanical strain using a Flexercell strain system significantly increased CD31-positive vascular structures and the angiogenesis guidance molecules plexinB1, ephrin B2, neuropilin1 (NRP1), semaphorin 4D (sem4D) and robo4 as well as vascular endothelial growth factor (VEGF), fibroblast growth factor-2 (FGF-2) and platelet-derived growth factor-BB (PDGF-BB) as evaluated by Western blot and real time RT-PCR...
December 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27720892/carbon-monoxide-releasing-molecule-induces-endothelial-nitric-oxide-synthase-activation-through-a-calcium-and-phosphatidylinositol-3-kinase-akt-mechanism
#13
Po-Min Yang, Yu-Ting Huang, Yu-Qi Zhang, Chia-Wen Hsieh, Being-Sun Wung
The production of nitric oxide (NO) by endothelial NO synthase (eNOS) plays a major role in maintaining vascular homeostasis. This study elucidated the potential role of carbon monoxide (CO)-releasing molecules (CORMs) in NO production and explored the underlying mechanisms in endothelial cells. We observed that 25μM CORM-2 could increase NO production and stimulate an increase in the intracellular Ca(2+) level. Furthermore, ethylene glycol-bis(β-aminoethyl ether)-N,N,N',N'-tetra acetic acid caused CORM-2-induced NO production, which was abolished by 1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid tetraacetoxy-methyl ester (BAPTA-AM), indicating that intracellular Ca(2+) release plays a major role in eNOS activation...
October 5, 2016: Vascular Pharmacology
https://www.readbyqxmd.com/read/27707506/fast-interaction-between-ampa-and-nmda-receptors-by-intracellular-calcium
#14
Andrei Rozov, Nail Burnashev
Suppression of NMDA receptor (NMDAR)-mediated currents by intracellular Ca(2+) has been described as a negative feedback loop in NMDAR modulation. In the time scale of tenths of milliseconds the depth of the suppression does not depend on the Ca(2+) source. It may be caused by Ca(2+) influx through voltage-gated calcium channels, NMDAR channels or release from intracellular stores. However, NMDARs are often co-expressed in synapses with Ca(2+)-permeable AMPA receptors (AMPARs). Due to significant differences in activation kinetics between these two types of glutamate receptors (GluRs), Ca(2+) entry through AMPARs precedes full activation of NMDARs, and therefore, might have an impact on the amplitude of NMDAR-mediated currents...
September 28, 2016: Cell Calcium
https://www.readbyqxmd.com/read/27703262/4-%C3%B0-minopyridine-sequesters-intracellular-ca-2-which-triggers-exocytosis-in-excitable-and-non-excitable-cells
#15
Ludmila A Kasatkina
4-aminopyridine is commonly used to stimulate neurotransmitter release resulting from sustained plasma membrane depolarization and Ca(2+)-influx from the extracellular space. This paper elucidated unconventional mechanism of 4-aminopyridine-stimulated glutamate release from neurons and non-neuronal cells which proceeds in the absence of external Ca(2+). In brain nerve terminals, primary neurons and platelets 4-aminopyridine induced the exocytotic release of glutamate that was independent of external Ca(2+) and was triggered by the sequestration of Ca(2+) from intracellular stores...
October 5, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27665314/role-of-subcellular-calcium-redistribution-in-regulating-apoptosis-and-autophagy-in-cadmium-exposed-primary-rat-proximal-tubular-cells
#16
Fei Liu, Zi-Fa Li, Zhen-Yong Wang, Lin Wang
Ca(2+) signaling plays a vital role in regulating apoptosis and autophagy. We previously proved that cytosolic Ca(2+) overload is involved in cadmium (Cd)-induced apoptosis in rat proximal tubular (rPT) cells, but the source of elevated cytosolic Ca(2+) concentration ([Ca(2+)]c) and the effect of potential subcellular Ca(2+) redistribution on apoptosis and autophagy remain to be elucidated. Firstly, data showed that Cd-induced elevation of [Ca(2+)]c was primarily generated intracellularly. Moreover, elevations of [Ca(2+)]c and mitochondrial Ca(2+) concentration ([Ca(2+)]mit) with depletion of endoplasmic reticulum (ER) Ca(2+) levels ([Ca(2+)]ER) were revealed in Cd-treated rPT cells, but this subcellular Ca(2+) redistribution was significantly suppressed by 2-Aminoethoxydiphenyl borate (2-APB)...
September 14, 2016: Journal of Inorganic Biochemistry
https://www.readbyqxmd.com/read/27640918/graphene-oxide-induces-apoptotic-cell-death-in-endothelial-cells-by-activating-autophagy-via-calcium-dependent-phosphorylation-of-c-jun-n-terminal-kinases
#17
Mi-Hee Lim, In Cheul Jeung, Jinyoung Jeong, Sung-Jin Yoon, Sang-Hyun Lee, Jongjin Park, Yu-Seon Kang, Hansu Lee, Young-Jun Park, Hee Gu Lee, Seon-Jin Lee, Baek Soo Han, Nam Woong Song, Sang Chul Lee, Jang-Seong Kim, Kwang-Hee Bae, Jeong-Ki Min
Despite the rapid expansion of the biomedical applications of graphene oxide (GO), safety issues related to GO, particularly with regard to its effects on vascular endothelial cells (ECs), have been poorly evaluated. To explore possible GO-mediated vasculature cytotoxicity and determine lateral GO size relevance, we constructed four types of GO: micrometer-sized GO (MGO; 1089.9 ± 135.3 nm), submicrometer-sized GO (SGO; 390.2 ± 51.4 nm), nanometer-sized GO (NGO; 65.5 ± 16.3 nm), and graphene quantum dots (GQDs)...
September 15, 2016: Acta Biomaterialia
https://www.readbyqxmd.com/read/27640744/mechanisms-underlying-effect-of-the-mycotoxin-cytochalasin-b-on-induction-of-cytotoxicity-modulation-of-cell-cycle-ca-2-homeostasis-and-ros-production-in-human-breast-cells
#18
Hong-Tai Chang, Chiang-Ting Chou, I-Shu Chen, Chia-Cheng Yu, Ti Lu, Shu-Shong Hsu, Pochuen Shieh, Chung-Ren Jan, Wei-Zhe Liang
Cytochalasin B, a cell-permeable mycotoxin isolated from the fungus Phoma spp., shows a wide range of biological effects, among which its potent antitumor activity has raised great interests in different models. However, the cytotoxic activity of cytochalasin B and its underlying mechanisms have not been elucidated in breast cells. This study examined the effect of cytochalasin B on MCF 10A human breast epithelial cells and ZR-75-1 human breast cancer cells. Cytochalasin B (10-20μM) concentration-dependently induced cytotoxicity, cell cycle arrest, and [Ca(2+)]i rises in ZR-75-1 cells but not in MCF 10A cells...
October 1, 2016: Toxicology
https://www.readbyqxmd.com/read/27627464/privileged-crosstalk-between-trpv1-channels-and-mitochondrial-calcium-shuttling-machinery-controls-nociception
#19
Iulia I Nita, Yaki Caspi, Sagi Gudes, Dimitri Fishman, Shaya Lev, Michal Hersfinkel, Israel Sekler, Alexander M Binshtok
The nociceptive noxious heat-activated receptor - TRPV1, conducts calcium and sodium, thus producing a depolarizing receptor potential, leading to activation of nociceptive neurons. TRPV1-mediated calcium and sodium influx is negatively modulated by calcium, via calcium-dependent desensitization of TRPV1 channels. A mitochondrial Ca(2+) uniporter - MCU, controls mitochondrial Ca(2+) entry while a sodium/calcium transporter - NCLX shapes calcium and sodium transients by mediating sodium entry into and removing calcium from the mitochondria...
December 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27608291/perturbation-of-akt-signaling-mitochondrial-potential-and-adp-atp-ratio-in-acidosis-challenged-rat-cortical-astrocytes
#20
King-Chuen Wu, Ka-Shun Cheng, Yu-Wen Wang, Yuh-Fung Chen, Kar-Lok Wong, Tzu-Hui Su, Paul Chan, Yuk-Man Leung
Cells switch to anaerobic glycolysis when there is a lack of oxygen during brain ischemia. Extracellular pH thus drops and such acidosis causes neuronal cell death. The fate of astrocytes, mechanical and functional partners of neurons, in acidosis is less studied. In this report we investigated the signaling in acidosis-challenged rat cortical astrocytes and whether these signals were related to mitochondrial dysfunction and cell death. Exposure to acidic pH (6.8, 6.0) caused Ca(2+) release and influx, p38 MAPK activation and Akt inhibition...
September 8, 2016: Journal of Cellular Biochemistry
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