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Wei Miao, Xiujuan Wu, Kang Wang, Wenjing Wang, Yumei Wang, Zhigang Li, Jingjing Liu, Li Li, Luying Peng
As a physiological small molecular product from the microbial fermentation of dietary fibers, butyrate plays an important role in maintaining intestinal health. Our previous works have proved that the effect of sodium butyrate (NaB) on the intestinal barrier function is mediated by activation of AMP-activated protein kinase (AMPK). However, the detailed pathway involved remains unknown. Using the calcium switch assay in the Caco-2 cell monolayer model, we found here that NaB activated AMPK mainly by increasing the calcium level, but not the ATP concentration, via promoting store-operated calcium entry (SOCE)...
October 10, 2016: International Journal of Molecular Sciences
Ming Wei, Yandong Zhou, Aomin Sun, Guolin Ma, Lian He, Lijuan Zhou, Shuce Zhang, Jin Liu, Shenyuan L Zhang, Donald L Gill, Youjun Wang
Store-operated Ca(2+) entry (SOCE) mediated by STIM1 and Orai1 is crucial for Ca(2+) signaling and homeostasis in most cell types. 2-Aminoethoxydiphenyl borate (2-APB) is a well-described SOCE inhibitor, but its mechanisms of action remain largely elusive. Here, we show that 2-APB does not affect the dimeric state of STIM1, but enhances the intramolecular coupling between the coiled-coil 1 (CC1) and STIM-Orai-activating region (SOAR) of STIM1, with subsequent reduction in the formation of STIM1 puncta in the absence of Orai1 overexpression...
October 10, 2016: Pflügers Archiv: European Journal of Physiology
Axel R Concepcion, Martin Vaeth, Larry E Wagner, Miriam Eckstein, Lee Hecht, Jun Yang, David Crottes, Maximilian Seidl, Hyosup P Shin, Carl Weidinger, Scott Cameron, Stuart E Turvey, Thomas Issekutz, Isabelle Meyts, Rodrigo S Lacruz, Mario Cuk, David I Yule, Stefan Feske
Eccrine sweat glands are essential for sweating and thermoregulation in humans. Loss-of-function mutations in the Ca2+ release-activated Ca2+ (CRAC) channel genes ORAI1 and STIM1 abolish store-operated Ca2+ entry (SOCE), and patients with these CRAC channel mutations suffer from anhidrosis and hyperthermia at high ambient temperatures. Here we have shown that CRAC channel-deficient patients and mice with ectodermal tissue-specific deletion of Orai1 (Orai1K14Cre) or Stim1 and Stim2 (Stim1/2K14Cre) failed to sweat despite normal sweat gland development...
October 10, 2016: Journal of Clinical Investigation
A Young Han, Hui Su Lee, Geun Hee Seol
This study assessed the effects of essential oil of Foeniculum vulgare Mill. (fennel oil) and of trans-anethole, the main component of fennel oil, on extracellular Ca(2+)-induced store-operated Ca(2+) entry (SOCE) into vascular endothelial (EA) cells and their mechanisms of action. Components of fennel oil were analyzed by gas chromatography-mass spectrometry. Cytosolic Ca(2+) concentration ([Ca(2+)]c) in EA cells was determined using Fura-2 fluorescence. In the presence of extracellular Ca(2+), fennel oil significantly increased [Ca(2+)]c in EA cells; this increase was significantly inhibited by the Ca(2+) channel blockers La(3+) and nifedipine...
October 6, 2016: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
Bo Lu, Marc Fivaz
Store-operated Ca(2+) entry (SOCE) is the primary Ca(2+) influx pathway in non-excitable cells. Long thought to be absent in nerve cells, neuronal SOCE is gaining popularity. We argue here that the evidence for SOCE in neurons remains contentious, mostly because SOCE imaging assays are inadequate in these cells.
October 5, 2016: Trends in Cell Biology
Ching Man Chan, Jacqueline T M Aw, Sarah E Webb, Andrew L Miller
In zebrafish embryos, distinct Ca2+ transients are localized to the early cleavage furrows during the first few cell division cycles. These transients are generated mainly by release via IP3Rs in the endoplasmic reticulum, and they are necessary for furrow positioning, propagation, deepening and apposition. We previously showed, via the use of inhibitors, that store-operated Ca2+ entry (SOCE) also appears to be essential for maintaining the IP3R-mediated elevated levels of [Ca2+]i for the extended periods required for the completion of successful furrow deepening and daughter cell apposition in these large embryonic cells...
October 5, 2016: Zygote: the Biology of Gametes and Early Embryos
Wei Rao, Cheng Peng, Lei Zhang, Ning Su, Kai Wang, Hao Hui, Shu-Hui Dai, Yue-Fan Yang, Peng Luo, Zhou Fei
Calcium disequilibrium is extensively involved in oxidative stress-induced neuronal injury. Although Homer1a is known to regulate several neuronal calcium pathways, its effects on, or its exact relationship with, oxidative stress-induced neuronal injury has not yet been fully elucidated. We found that Homer1a protected HT-22 cells from glutamate-induced oxidative stress injury by inhibiting final-phase intracellular calcium overload and mitochondrial oxidative stress. In these cells, stromal interactive molecule 1 (STIM1) puncta, but not the protein level, was significantly increased after glutamate treatment...
September 29, 2016: Scientific Reports
Lisha Qi, Wangzhao Song, Lingmei Li, Lu Cao, Yue Yu, Chunmin Song, Yalei Wang, Fei Zhang, Yang Li, Bin Zhang, Wenfeng Cao
Several fibroblast growth factor (FGF) isoforms act to stimulate epithelial-mesenchymal transition (EMT) during cancer progression. FGF4 and FGF7 are two ligands of FGF receptor 2 (FGFR2). Using two lung adenocarcinoma (ADC) cell lines, A549 and H1299, we showed that FGF4, but not FGF7, altered cell morphology, promoted EMT-associated protein expression, and enhanced cell proliferation, migration/invasion and colony initiation. In addition, FGF4 increased store-operated calcium entry (SOCE) and expression of the calcium signal-associated protein Orai1...
September 22, 2016: Oncotarget
Clark A Briggs, Shreaya Chakroborty, Grace E Stutzmann
The current state of the AD research field is highly dynamic is some respects, while seemingly stagnant in others. Regarding the former, our current lack of understanding of initiating disease mechanisms, the absence of effective treatment options, and the looming escalation of AD patients is energizing new research directions including a much-needed re-focusing on early pathogenic mechanisms, validating novel targets, and investigating relevant biomarkers, among other exciting new efforts to curb disease progression and foremost, preserve memory function...
September 20, 2016: Biochemical and Biophysical Research Communications
Judith A Stolwijk, Xuexin Zhang, Maxime Gueguinou, Wei Zhang, Khalid Matrougui, Christian Renken, Mohamed Trebak
Endothelial barrier function is tightly regulated by plasma membrane receptors and is crucial for tissue fluid homeostasis; its dysfunction causes disease, including sepsis and inflammation. The ubiquitous activation of Ca2+ signaling upon phospholipase C (PLC)-coupled receptor ligation leads quite naturally to the assumption that Ca2+ signaling is required for receptor-regulated endothelial barrier function. This widespread hypothesis draws analogy from smooth muscle and proposes the requirement of G protein coupled receptor (GPCR)-generated Ca2+ signaling in activating the endothelial contractile apparatus and generating inter-endothelial gaps...
September 13, 2016: Journal of Biological Chemistry
Vijaya Lakshmi Bodiga, Santhi Priya Inapurapu, Praveen Kumar Vemuri, Madhukar Rao Kudle, Sreedhar Bodiga
Platinum-based chemotherapeutic regimen induces vascular dysfunction. Action of cisplatin on endothelial cells is mediated by protein kinase C (PKC-α), which further activates nuclear factor-κB (NF-κB) and induces canonical transient receptor potential channel (TRPC1) and intercellular adhesion molecule (ICAM-1) expression. Increased ICAM-1 contributes to hyperadhesion of monocytes and endothelial dysfunction. PKC-α is also involved in phosphorylation of TRPC1, resulting in store-operated calcium entry (SOCE) and further activation of NF-κB...
September 8, 2016: European Journal of Pharmacology
Shaqiu Zhang, Tamer Al-Maghout, Yuetao Zhou, Rosi Bissinger, Abeer Abousaab, Madhuri S Salker, Lisann Pelzl, Bradley S Cobb, Anchun Cheng, Yogesh Singh, Florian Lang
BACKGROUND/AIMS: Activation of T cell receptors (TCRs) in CD4+ T cells leads to a cascade of signalling reactions including increase of intracellular calcium (Ca2+) levels with subsequent Ca2+ dependent stimulation of gene expression, proliferation, cell motility and cytokine release. The increase of cytosolic Ca2+ results from intracellular Ca2+ release with subsequent activation of store-operated Ca2+ entry (SOCE). Previous studies suggested miRNAs are required for the development and functions of CD4+ T cells...
2016: Cellular Physiology and Biochemistry
Benjamin Chun-Kit Tong, Claire Shuk-Kwan Lee, Wing-Hei Cheng, Kwok-On Lai, J Kevin Foskett, King-Ho Cheung
Some forms of familial Alzheimer's disease (FAD) are caused by mutations in presenilins (PSs), catalytic components of a γ-secretase complex that cleaves target proteins, including amyloid precursor protein (APP). Calcium (Ca(2+)) dysregulation in cells with these FAD-causing PS mutants has been attributed to attenuated store-operated Ca(2+) entry [SOCE; also called capacitative Ca(2+) entry (CCE)]. CCE occurs when STIM1 detects decreases in Ca(2+) in the endoplasmic reticulum (ER) and activates ORAI channels to replenish Ca(2+) stores in the ER...
2016: Science Signaling
Sumita Chakraborty, Bipan K Deb, Tetyana Chorna, Vera Konieczny, Colin W Taylor, Gaiti Hasan
Store-operated Ca(2+) entry (SOCE) occurs when loss of Ca(2+) from the endoplasmic reticulum (ER) stimulates the Ca(2+) sensor, STIM, to cluster and activate the plasma membrane Ca(2+) channel Orai (encoded by Olf186-F in flies). Inositol 1,4,5-trisphosphate receptors (IP3Rs, which are encoded by a single gene in flies) are assumed to regulate SOCE solely by mediating ER Ca(2+) release. We show that in Drosophila neurons, mutant IP3R attenuates SOCE evoked by depleting Ca(2+) stores with thapsigargin. In normal neurons, store depletion caused STIM and the IP3R to accumulate near the plasma membrane, association of STIM with Orai, clustering of STIM and Orai at ER-plasma-membrane junctions and activation of SOCE...
October 15, 2016: Journal of Cell Science
G Y Peng, J Xu, R M Liu, W Hong, X M He, Y E Lin
OBJECTIVE: To determine whether store-operated Ca(2+) entry (SOCE) is involved in chronic hypoxia-induced alteration of intracellular Ca(2+) concentration ([Ca(2+) ]i) and proliferation in pulmonary arterial smooth muscle cells (PASMC). METHODS: Rat PASMCs were cultured and treated in normoxia (21%O2) or hypoxia (4%O2) condition. The proliferation of PASMC was detected by cell counting kit-8 (CCK-8) assay. [Ca(2+) ]i, SOCE and the effects of store-operated Ca(2+) channel (SOCC) inhibitors, SKF96365 and NiCl2, on SOCE in hypoxic PASMCs were tested by InCyte [Ca(2+) ]i measurement system...
September 1, 2016: Zhonghua Nei Ke za Zhi [Chinese Journal of Internal Medicine]
Magdalena Czeredys, Filip Maciąg, Axel Methner, Jacek Kuźnicki
Huntington's disease (HD) is a hereditary neurodegenerative disease caused by a polyglutamine expansion within the huntingtin (HTT) gene. One of the cellular functions that is dysregulated in HD is store-operated calcium entry (SOCE), a process in which the depletion of Ca(2+) from the endoplasmic reticulum (ER) induces Ca(2+) influx from the extracellular space. We detected an enhanced activity of SOC channels in medium spiny neurons (MSNs) from YAC128 mice, a transgenic model of HD, and investigated whether this could be reverted by tetrahydrocarbazoles...
August 20, 2016: Biochemical and Biophysical Research Communications
Tomasz Wegierski, Kinga Gazda, Jacek Kuznicki
Familial Alzheimer's disease (FAD)-causing mutations in presenilins were shown to alter intracellular calcium dynamics, including store-operated calcium entry (SOCE). However, the involvement of FAD-linked amyloid precursor protein (APP) in SOCE remains controversial. Here, we used gain-of-function and loss-of-function approaches to shed light on this issue. We found that Jurkat cells, which exhibit prominent SOCE mediated by Orai channels, maintain low APP levels. The ectopic expression of APP, either with wildtype sequence or FAD-causing Swedish mutation, had no effect on SOCE induced by calcium store depletion with cyclopiazonic acid (CPA)...
September 23, 2016: Biochemical and Biophysical Research Communications
Catherine A Rivet, Ariel S Kniss-James, Margaret A Gran, Anish Potnis, Abby Hill, Hang Lu, Melissa L Kemp
T cells reach a state of replicative senescence characterized by a decreased ability to proliferate and respond to foreign antigens. Calcium release associated with TCR engagement is widely used as a surrogate measure of T cell response. Using an ex vivo culture model that partially replicates features of organismal aging, we observe that while the amplitude of Ca2+ signaling does not change with time in culture, older T cells exhibit faster Ca2+ rise and a faster decay. Gene expression analysis of Ca2+ channels and pumps expressed in T cells by RT-qPCR identified overexpression of the plasma membrane CRAC channel subunit ORAI1 and PMCA in older T cells...
2016: PloS One
Stacey Dineen Rodenbeck, Chad A Zarse, Mikaela L McKenney-Drake, Rebecca S Bruning, Michael Sturek, Neal X Chen, Sharon M Moe
BACKGROUND: Vascular smooth muscle cells (VSMCs) exhibit phenotypic plasticity, promoting vascular calcification and increasing cardiovascular risk. Changes in VSMC intracellular calcium ([Ca(2+)]i) are a major determinant of plasticity, but little is known about changes in [Ca(2+)]i in chronic kidney disease (CKD). We have previously demonstrated such plasticity in aortas from our rat model of CKD and therefore sought to examine changes in [Ca(2+)]i during CKD progression. MATERIALS AND METHODS: We examined freshly isolated VSMCs from aortas of normal rats, Cy/+ rats (CKD) with early and advanced CKD, and advanced CKD rats treated without and with 3% calcium gluconate (CKD + Ca(2+)) to lower parathyroid hormone (PTH) levels...
August 9, 2016: Nephrology, Dialysis, Transplantation
Letizia Albarrán, José J López, Luis J Gómez, Ginés M Salido, Juan A Rosado
Canonical transient receptor potential-1 (TRPC1) is an almost ubiquitously expressed channel that plays a relevant role in cell function. As other TRPC members, TRPC1 forms receptor-operated cation channels that exhibit both STIM1-dependent and store-independent behaviour. The STIM1 inhibitor SARAF (for store-operated Ca(2+) entry (SOCE)-associated regulatory factor) modulates SOCE by interaction with the STIM1 region responsible for Orai1 activation (SOAR). Furthermore, SARAF modulates Ca(2+) entry through the arachidonate-regulated Ca(2+) (ARC) channels, consisting of Orai1 and Orai3 heteropentamers and plasma membrane-resident STIM1...
October 15, 2016: Biochemical Journal
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