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https://www.readbyqxmd.com/read/29352220/soce-induced-calcium-overload-regulates-autophagy-in-acute-pancreatitis-via-calcineurin-activation
#1
Zhen-Dong Zhu, Tao Yu, Hua-Jing Liu, Jing Jin, Jun He
Acute pancreatitis (AP) is an acute inflammatory process of the pancreas that is characterized by inflammation, edema, vacuolization and necrosis, which has significant morbidity and lethality. The pathogenesis of AP has not been established completely. An early and critical feature of AP is the aberrant signaling of Calcium (Ca2+) within the pancreatic acinar cell, termed Ca2+ overload. Store-operated Ca2+ (SOC) channels are the principal Ca2+ influx channels that contribute to Ca2+ overload in pancreatic acinar cells...
January 19, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29351410/hypoxia-selectively-upregulates-cation-channels-and-increases-cytosolic-ca2-in-pulmonary-but-not-coronary-arterial-smooth-muscle-cells
#2
Xi He, Shanshan Song, Ramon J Ayon, Angela Balisterieri, Stephen M Black, Ayako Makino, W Gil Wier, Wei-Jin Zang, Jason X-J Yuan
Ca2+ signaling, particularly the mechanism via store-operated Ca2+ entry (SOCE) and receptor-operated Ca2+ entry (ROCE), plays a critical role in the development of acute hypoxia-induced pulmonary vasoconstriction and chronic hypoxia-induced pulmonary hypertension. This study aimed to test the hypothesis that chronic hypoxia differentially regulates the expression of proteins that mediate SOCE and ROCE (STIM, Orai, and TRPC6) in pulmonary (PASMC) and coronary (CASMC) artery smooth muscle cells. The resting cytosolic [Ca2+] ([Ca2+]cyt) and the stored [Ca2+] in the sarcoplasmic reticulum (SR) were not different in CASMC and PASMC...
January 3, 2018: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/29347889/allostery-in-orai1-binding-to-calmodulin-revealed-from-conformational-thermodynamics
#3
Lakshmi Maganti, Sutapa Dutta, Mahua Ghosh, J Chakrabarti
Here we study microscopic mechanism of complex formation between Ca2+ bound -calmodulin (holoCaM) and Orai1 that regulates Ca2+-dependent inactivation process in eukaryotic cells. We compute conformational thermodynamic changes in holoCaM with respect to complex of Orai1 bound to C-terminal domain of holoCaM using histograms of dihedral angles of the proteins over trajectories from molecular dynamics simulations. Our analysis shows that the N-terminal domain residues L4, T5, Q41, N42, T44 and E67 of holoCaM get destabilized and disordered due to Orai1 binding to C-terminal domain of calmodulin affect the N-terminal domain residues...
January 18, 2018: Journal of Biomolecular Structure & Dynamics
https://www.readbyqxmd.com/read/29337674/a-study-on-blocking-store-operated-ca2-entry-in-pulmonary-arterial-smooth-muscle-cells-with-xyloketals-from-marine-fungi
#4
Jie-Bin Zhou, Ying-Ying Sun, Ying-Lin Zheng, Chu-Qin Yu, Hua-Qing Lin, Ji-Yan Pang
In this study, the effect of four xyloketals 1-4 on store-operated calcium entry (SOCE) was investigated in primary distal pulmonary arterial smooth muscle cells (PASMCs) isolated from mice. The results showed that xyloketal A (1), an unusual ketal with C-3 symmetry, exhibited strong SOCE blocking activity. Secretion of interleukin-8 (IL-8) was also inhibited by xyloketal A. The parallel artificial membrane permeability assay (PAMPA) of 1-4 suggested that these xyloketals penetrated easily through the cell membrane...
December 20, 2017: Acta Pharmaceutica
https://www.readbyqxmd.com/read/29335300/extracellular-atp-activates-store-operated-ca2-entry-in-white-adipocytes-functional-evidence-for-stim1-and-orai1
#5
Mickaël F El Hachmane, Anna Ermund, Cecilia Brännmark, Charlotta S Olofsson
Here we have applied ratiometric measurements of intracellular Ca2+ concentrations ([Ca2+]i) to show that extracellularly applied ATP (100 mM) stimulates store-operated Ca2+ entry (SOCE) in 3T3-L1 adipocytes. ATP produced a rapid increase in [Ca2+]i consisting of an initial transient elevation followed by a sustained elevated phase that could be observed only in the presence of extracellular Ca2+ Gene expression data and [Ca2+]i recordings with uridine-5'-triphosphate (UTP) or with the phospholipase C (PLC) inhibitor U73122 demonstrated the involvement of purinergic P2Y2 receptors and the PLC/inositol trisphosphate (IP3) pathway...
January 15, 2018: Biochemical Journal
https://www.readbyqxmd.com/read/29324706/endothelial-ca2-signaling-and-the-resistance-to-anticancer-treatments-partners-in-crime
#6
REVIEW
Francesco Moccia
Intracellular Ca2+ signaling drives angiogenesis and vasculogenesis by stimulating proliferation, migration, and tube formation in both vascular endothelial cells and endothelial colony forming cells (ECFCs), which represent the only endothelial precursor truly belonging to the endothelial phenotype. In addition, local Ca2+ signals at the endoplasmic reticulum (ER)-mitochondria interface regulate endothelial cell fate by stimulating survival or apoptosis depending on the extent of the mitochondrial Ca2+ increase...
January 11, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29316690/vsp-17-a-new-ppar%C3%AE-agonist-suppresses-the-metastasis-of-triple-negative-breast-cancer-via-upregulating-the-expression-of-e-cadherin
#7
Yuhui Wang, Menglin Zhu, Bo Yuan, Kefeng Zhang, Mingli Zhong, Wei Yi, Xiaotian Xu, Xiaoqun Duan
Triple-negative breast cancer (TNBC), an aggressive subtype of breast cancer, shows higher metastases and relapse rates than other subtypes. The metastasis of TNBC is the main reason for the death of TNBC patients. Increasing evidence has shown that inhibiting the metastasis of TNBC is a good method for TNBC treatment. Here, VSP-17 was designed and synthesized as an agonist of PPARγ, evidenced by upregulating the expression of CD36 and increasing the activity of PPARγ reporter gene. VSP-17 obviously inhibited the migration and invasion process of MDA-MB-231 cells but showed little effect on the viability of MDA-MB-231 cells...
January 8, 2018: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
https://www.readbyqxmd.com/read/29307746/orai1-is-critical-for-notch-driven-aggressiveness-under-hypoxic-conditions-in-triple-negative-breast-cancers
#8
Xiaoyu Liu, Teng Wang, Yan Wang, Zhen Chen, Dong Hua, Xiaoqiang Yao, Xin Ma, Peng Zhang
It is believed that hypoxia stimulates triple-negative breast cancers (TNBCs) metastasis, which is associated with a poor prognosis. However, the underlying mechanism remains unclear. Here, we demonstrated that hypoxia up-regulates both the levels of Orai1 and Notch1, and the increase in Orai1 is mediated by Notch1 signaling in TNBCs. Functionally, Orai1 caused a sustained elevation of intracellular Ca2+ via Store-operated Ca2+ entry (SOCE), then activated the calcineurin-nuclear factor of activated T-cell 4 (NFAT4, also named NFATc3) in hypoxic TNBCs...
January 4, 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29306759/il-4-and-serum-amyloid-p-inversely-regulate-fibrocyte-differentiation-by-targeting-store-operated-ca2-channels
#9
Jin-Nan Zhong, Lan Lan, Yi-Fei Chen, Ge Huang, Guang-Zhen He, Jiong Yang, Ya-Dong Gao
BACKGROUND: Circulating fibrocytes (CFs) have been shown to participate in subepithelial fibrosis of asthma with chronic airflow limitation by acting as an important source of fibroblasts deposited beneath airway epithelia. Serum amyloid P (SAP) is an innate inhibitor of fibrocytes differentiation. Store-operated Ca2+ entry (SOCE) is the major Ca2+ influx of non-excitable cells. In this study, the role of SOCE in the regulation of fibrocytes differentiation and the effects of Th2 cytokine IL-4 and SAP on SOCE of fibrocytes were investigated...
July 12, 2017: Pharmacological Reports: PR
https://www.readbyqxmd.com/read/29305862/stim1-deficiency-protects-the-liver-from-ischemia-reperfusion-injury-in-mice
#10
Yanyang Li, Chunyan Lou, Weiying Wang
Hepatic ischemia reperfusion (I/R) injury is unavoidable in various clinical conditions. Despite considerable investigation, the underlying molecular mechanism revealing liver I/R injury remains elusive. Stromal interaction molecule 1 (STIM1) plays essential role in regulating the induction of cellular responses to a number of stress conditions, including temperature changes, elevated ROS, and hypoxia. Here, to explore if STIM1 is involved in hepatic injury, wild type (WT) and STIM1-knockout (STIM1-/-) mice were subjected to I/R...
January 3, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29298434/coiled-coil-formation-conveys-a-stim1-signal-from-er-lumen-to-cytoplasm
#11
Nupura Hirve, Vangipurapu Rajanikanth, Patrick G Hogan, Aparna Gudlur
STIM1 and STIM2 are endoplasmic reticulum (ER) membrane proteins that sense decreases in ER-luminal free Ca2+ and, through a conformational change in the STIM cytoplasmic domain, control gating of the plasma membrane Ca2+ channel ORAI1. To determine how STIM1 conveys a signal from the ER lumen to the cytoplasm, we studied the Ca2+-dependent conformational change of engineered STIM1 proteins in isolated ER membranes and, in parallel, physiological activation of these proteins in cells. We find that conserved "sentinel" features of the CC1 region help to prevent activation while Ca2+ is bound to STIM ER-luminal domains...
January 2, 2018: Cell Reports
https://www.readbyqxmd.com/read/29284605/filamin-a-modulates-store-operated-ca2-entry-by-regulating-stim1-stromal-interaction-molecule-1-orai1-association-in-human-platelets
#12
Jose J Lopez, Letizia Albarrán, Isaac Jardín, Jose Sanchez-Collado, Pedro C Redondo, Nuria Bermejo, Regis Bobe, Tarik Smani, Juan A Rosado
OBJECTIVE: Here, we provide evidence for the role of FLNA (filamin A) in the modulation of store-operated calcium entry (SOCE). APPROACH AND RESULTS: SOCE is a major mechanism for calcium influx controlled by the intracellular Ca2+ stores. On store depletion, the endoplasmic reticulum calcium sensor STIM1 (stromal interaction molecule 1) redistributes into puncta at endoplasmic reticulum/plasma membrane junctions, a process supported by the cytoskeleton, where it interacts with the calcium channels; however, the mechanism for fine-tuning SOCE is not completely understood...
December 28, 2017: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/29242293/variable-impairment-of-platelet-functions-in-patients-with-severe-genetically-linked-immune-deficiencies
#13
Magdolna Nagy, Tom G Mastenbroek, Nadine J A Mattheij, Susanne de Witt, Kenneth J Clemetson, Janbernd Kirschner, Ansgar S Schulz, Thomas Vraetz, Carsten Speckmann, Attila Braun, Judith M E M Cosemans, Barbara Zieger, Johan W M Heemskerk
In patients with dysfunctions of the Ca2+ channel ORAI1, stromal interaction molecule 1 (STIM1) or integrin-regulating kindlin-3 (FERMT3), severe immunodeficiency is frequently linked to abnormal platelet activity. In this paper, we studied in nine rare patients, including relatives, with confirmed genetic mutations of ORAI1, STIM1 or FERMT3, platelet responsiveness by multi-parameter assessment of whole blood thrombus formation under high-shear flow conditions. In platelets isolated from 5 out of 6 patients with ORAI1 or STIM1 mutations, store-operated Ca2+ entry (SOCE) was (in)completely defective compared to control platelets...
December 14, 2017: Haematologica
https://www.readbyqxmd.com/read/29241198/fam3a-protects-against-glutamate-induced-toxicity-by-preserving-calcium-homeostasis-in-differentiated-pc12-cells
#14
Qing Song, Wen-Li Gou, Yu-Liang Zou
BACKGROUND/AIMS: Stroke is the leading cause of adult disability, and glutamate-induced dysregulation of intracellular Ca2+ homeostasis is a key mechanism. FAM3A is the first member of the family with sequence similarity 3 (FAM3) gene family, and its biological function remains largely unknown. We have recently reported that FAM3A exerts protective effects against oxidative stress and mitochondrial dysfunction in HT22 cells. METHODS: Here, we investigated the protective effects of FAM3A using a glutamate-induced neuronal injury model in nerve growth factor (NGF)-differentiated PC12 cells...
December 12, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29239723/intermittent-ca2-signals-mediated-by-orai1-regulate-basal-t-cell-motility
#15
Tobias X Dong, Shivashankar Othy, Milton L Greenberg, Amit Jairaman, Chijioke Akunwafo, Sabrina Leverrier, Ying Yu, Ian Parker, Joseph L Dynes, Michael D Cahalan
Ca2+ influx through Orai1 channels is crucial for several T cell functions, but a role in regulating basal cellular motility has not been described. Here we show that inhibition of Orai1 channel activity increases average cell velocities by reducing the frequency of pauses in human T cells migrating through confined spaces, even in the absence of extrinsic cell contacts or antigen recognition. Utilizing a novel ratiometric genetically encoded cytosolic Ca2+ indicator, Salsa6f, which permits real-time monitoring of cytosolic Ca2+ along with cell motility, we show that spontaneous pauses during T cell motility in vitro and in vivo coincide with episodes of cytosolic Ca2+ signaling...
December 14, 2017: ELife
https://www.readbyqxmd.com/read/29237734/authentic-crac-channel-activity-requires-stim1-and-the-conserved-portion-of-the-orai-n-terminus
#16
Isabella Derler, Carmen Butorac, Adela Krizova, Michael Stadlbauer, Martin Muik, Marc Fahrner, Irene Frischauf, Christoph Romanin
Calcium (Ca2+) is an essential second messenger required for diverse signaling processes in immune cells. Ca2+ release-activated Ca2+ (CRAC) channels represent one main Ca2+ entry pathway into the cell. They are fully reconstituted via two proteins, the stromal interaction molecule 1 (STIM1), a Ca2+ sensor in the endoplasmic reticulum and the Ca2+ ion channel Orai in the plasma membrane. After Ca2+ store depletion, STIM1 and Orai couple to each other allowing Ca2+ influx. CRAC-/STIM1-mediated Orai channel currents display characteristic hallmarks such as high Ca2+ selectivity, an increase in current density when switching from a Ca2+-containing solution to a divalent-free Na+ one and fast Ca2+ dependent inactivation...
December 13, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29237733/communication-between-n-terminus-and-loop2-tunes-orai-activation
#17
Marc Fahrner, Saurabh K Pandey, Martin Muik, Lukas Traxler, Carmen Butorac, Michael Stadlbauer, Vasilina Zayats, Adéla Krizova, Peter Plenk, Irene Frischauf, Rainer Schindl, Hermann J Gruber, Peter Hinterdorfer, Rüdiger Ettrich, Christoph Romanin, Isabella Derler
Ca2+ release-activated Ca2+ (CRAC) channels constitute the major Ca2+ entry pathway into the cell. They are fully reconstituted via intermembrane coupling of the Ca2+ selective Orai channel and the Ca2+ sensing protein STIM1. In addition to the Orai C-terminus, the main coupling site for STIM1, the Orai N-terminus is indispensable for Orai channel gating. Although the extended transmembrane Orai N-terminal (ETON) region (Orai1: aa73-91; Orai3: aa48-65) is fully conserved in the Orai1 and Orai3 isoforms, Orai3 tolerates larger N-terminal truncations than Orai1 in retaining store-operated activation...
December 13, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29230527/lefty2-inhibits-endometrial-receptivity-by-downregulating-orai1-expression-and-store-operated-ca2-entry
#18
Madhuri S Salker, Yogesh Singh, Ruban R Peter Durairaj, Jing Yan, Md Alauddin, Ni Zeng, Jennifer H Steel, Shaqiu Zhang, Jaya Nautiyal, Zoe Webster, Sara Y Brucker, Diethelm Wallwiener, B Anne Croy, Jan J Brosens, Florian Lang
Early embryo development and endometrial differentiation are initially independent processes, and synchronization, imposed by a limited window of implantation, is critical for reproductive success. A putative negative regulator of endometrial receptivity is LEFTY2, a member of the transforming growth factor (TGF)-β family. LEFTY2 is highly expressed in decidualizing human endometrial stromal cells (HESCs) during the late luteal phase of the menstrual cycle, coinciding with the closure of the window of implantation...
December 11, 2017: Journal of Molecular Medicine: Official Organ of the "Gesellschaft Deutscher Naturforscher und Ärzte"
https://www.readbyqxmd.com/read/29229703/orai1-plays-a-crucial-role-in-central-sensitization-by-modulating-neuronal-excitability
#19
Yannong Dou, Jingsheng Xia, Ruby Gao, Xinghua Gao, Frances M Munoz, Dongyu Wei, Yuzhen Tian, James E Barrett, Seena Ajit, Olimpia Meucci, James W Putney, Yue Dai, Huijuan Hu
Pathological pain is a common and debilitating condition that is often poorly managed. Central sensitization is an important mechanism underlying pathological pain. However, candidate molecules involved in central sensitization remain unclear. Store-operated calcium channels (SOCs) mediate important calcium signals in non-excitable and excitable cells. SOCs have been implicated in a wide variety of human pathophysiological conditions including immunodeficiency, occlusive vascular diseases and cancer. However, the role of SOCs in central nervous system (CNS) disorders has been relatively unexplored...
December 11, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29225169/inhibition-of-orai1-mediated-ca2-entry-limits-endothelial-cell-inflammation-by-suppressing-calcineurin-nfatc4-signaling-pathway
#20
Bei-Xin Yu, Jia-Ni Yuan, Fei-Ran Zhang, Ying-Ying Liu, Ting-Ting Zhang, Kai Li, Xiao-Fei Lv, Jia-Guo Zhou, Lin-Yan Huang, Jin-Yan Shang, Si-Jia Liang
Orai1-dependent Ca2+ entry plays an essential role in inflammatory response through regulating T cell and macrophage activation and neutrophil infiltration. However, whether Orai1 Ca2+ entry contributes to endothelial activation, one of the early steps of vascular inflammation, remains elusive. In the present study, we observed that knockdown of Orai1 reduced, whereas overexpression of Orai1 potentiated, TNFα-induced expression of adhesion molecules such as ICAM-1 and VCAM-1 in HUVECs, and subsequently blocked adhesion of monocyte to HUVECs...
December 7, 2017: Biochemical and Biophysical Research Communications
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