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https://www.readbyqxmd.com/read/29306759/il-4-and-serum-amyloid-p-inversely-regulate-fibrocyte-differentiation-by-targeting-store-operated-ca2-channels
#1
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/29284605/filamin-a-modulates-store-operated-ca2-entry-by-regulating-stim1-stromal-interaction-molecule-1-orai1-association-in-human-platelets
#2
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/29284321/ral-function-in-muscle-is-required-for-flight-maintenance-in-drosophila
#3
Shlesha Richhariya, Gaiti Hasan
Ral is a small GTPase of the Ras superfamily that is important for a number of cellular functions. Recently, we found that expression of Ral is regulated by store-operated calcium entry (SOCE) in Drosophila neurons. In this study, through genetic and behavioural experiments, we show that Ral function is required in differentiated muscles for flight. Reducing Ral function in muscles, specifically reduced duration of flight bouts but not other motor functions, like climbing. Interestingly, unlike in the nervous system, Ral expression in the muscle is not regulated by SOCE...
December 28, 2017: Small GTPases
https://www.readbyqxmd.com/read/29273760/urotensin-ii-induced-store-operated-ca2-entry-contributes-to-glomerular-mesangial-cell-proliferation-and-extracellular-matrix-protein-production-under-high-glucose-conditions
#4
Hitesh Soni, Adebowale Adebiyi
Glomerular mesangial cell (GMC) proliferation and matrix expansion are pathological hallmarks of a wide range of kidney diseases, including diabetic nephropathy. Although the circulating level of peptide hormone urotensin II (UII) and kidney tissue expression of UII and UII receptors (UTR) are increased in diabetic nephropathy, it remains unclear whether UII regulates GMC growth and extracellular matrix (ECM) accumulation. In this study, we tested the hypothesis that UII-induced Ca2+ signaling controls GMC proliferation and ECM production under normal and high glucose conditions...
December 22, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29243846/aqp2-can-modulate-the-pattern-of-ca2-transients-induced-by-store-operated-ca2-entry-under-trpv4-activation
#5
Alejandro Pizzoni, Macarena López González, Gisela Di Giusto, Valeria Rivarola, Claudia Capurro, Paula Ford
There is increasing evidence indicating that aquaporins (AQPs) exert an influence in cell signaling by the interplay with the TRPV4 Ca2+ channel. Ca2+ release from intracellular stores and plasma membrane hyperpolarization due to opening of Ca2+ -activated potassium channels (KCa) are events that have been proposed to take place downstream of TRPV4 activation. A major mechanism for Ca2+ entry, activated after depletion of intracellular Ca2+ stores and driven by electrochemical forces, is the store-operated Ca2+ entry (SOCE)...
December 15, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/29243589/defective-stim-mediated-store-operated-ca2-entry-in-hepatocytes-leads-to-metabolic-dysfunction-in-obesity
#6
Ana Paula Arruda, Benedicte Mengel Pers, Günes Parlakgul, Ekin Güney, Ted Goh, Erika Cagampan, Grace Yankun Lee, Renata L Goncalves, Gökhan S Hotamisligil
Defective Ca2+ handling is a key mechanism underlying hepatic endoplasmic reticulum (ER) dysfunction in obesity. ER Ca2+ level is in part monitored by the store-operated Ca2+ entry (SOCE) system, an adaptive mechanism that senses ER luminal Ca2+ concentrations through the STIM proteins and facilitates import of the ion from the extracellular space. Here, we show that hepatocytes from obese mice displayed significantly diminished SOCE as a result of impaired STIM1 translocation, which was associated with aberrant STIM1 O-GlycNAcylation...
December 15, 2017: ELife
https://www.readbyqxmd.com/read/29242293/variable-impairment-of-platelet-functions-in-patients-with-severe-genetically-linked-immune-deficiencies
#7
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
#8
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/29230527/lefty2-inhibits-endometrial-receptivity-by-downregulating-orai1-expression-and-store-operated-ca2-entry
#9
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/29223474/fine-tuning-of-store-operated-calcium-entry-by-fast-and-slow-ca2-dependent-inactivation-involvement-of-saraf
#10
REVIEW
Isaac Jardín, Letizia Albarran, Ginés M Salido, Jose J López, Stewart O Sage, Juan A Rosado
Store-operated Ca2+ entry (SOCE) is a functionally relevant mechanism for Ca2+ influx present in electrically excitable and non-excitable cells. Regulation of Ca2+ entry through store-operated channels is essential to maintain an appropriate intracellular Ca2+ homeostasis and prevent cell damage. Calcium-release activated channels exhibit Ca2+-dependent inactivation mediated by two temporally separated mechanisms: fast Ca2+-dependent inactivation takes effect in the order of milliseconds and involves the interaction of Ca2+ with residues in the channel pore while slow Ca2+-dependent inactivation (SCDI) develops over tens of seconds, requires a global rise in [Ca2+]cyt and is a mechanism regulated by mitochondria...
December 6, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29221123/vegf-induced-intracellular-ca2-oscillations-are-down-regulated-and-do-not-stimulate-angiogenesis-in-breast-cancer-derived-endothelial-colony-forming-cells
#11
Francesco Lodola, Umberto Laforenza, Fabio Cattaneo, Federico Alessandro Ruffinatti, Valentina Poletto, Margherita Massa, Richard Tancredi, Estella Zuccolo, Dlzar Alì Khdar, Alberto Riccardi, Marco Biggiogera, Vittorio Rosti, Germano Guerra, Francesco Moccia
Endothelial colony forming cells (ECFCs) represent a population of truly endothelial precursors that promote the angiogenic switch in solid tumors, such as breast cancer (BC). The intracellular Ca2+ toolkit, which drives the pro-angiogenic response to VEGF, is remodelled in tumor-associated ECFCs such that they are seemingly insensitive to this growth factor. This feature could underlie the relative failure of anti-VEGF therapies in cancer patients. Herein, we investigated whether and how VEGF uses Ca2+ signalling to control angiogenesis in BC-derived ECFCs (BC-ECFCs)...
November 10, 2017: Oncotarget
https://www.readbyqxmd.com/read/29212003/soce-is-important-for-maintaining-sarcoplasmic-calcium-content-and-release-in-skeletal-muscle-fibers
#12
Mónika Sztretye, Nikolett Geyer, János Vincze, Dána Al-Gaadi, Tamás Oláh, Péter Szentesi, Gréta Kis, Miklós Antal, Ildikó Balatoni, László Csernoch, Beatrix Dienes
Store-operated Ca2+ entry (SOCE) is a Ca2+-entry process activated by the depletion of intracellular stores and has an important role in many cell types. In skeletal muscle, however, its role during physiological muscle activation has been controversial. To address this question, sarcoplasmic reticulum (SR) calcium release in a mouse strain with a naturally occurring mutation in the myostatin gene (Compact (Cmpt)) leading to a hypermuscular yet reduced muscle-force phenotype was compared to that in wild-type mice...
December 5, 2017: Biophysical Journal
https://www.readbyqxmd.com/read/29210464/ca2-and-lipid-signals-hold-hands-at-er-plasma-membrane-contact-sites
#13
Tamas Balla
Discovery of the STIM1 and Orai proteins as the principal components of store-operated Ca2+ entry (SOCE) has drawn attention to contact sites between the ER and the plasma membrane (PM). Such contacts between adjacent membranes of different cellular organelles, primarily between the mitochondria and the ER, had already been known as the sites where Ca2+ released from the ER can be efficiently channeled to the mitochondria and also where phosphatidylserine synthesis and transfer takes place. Recent studies have identified contact sites between virtually every organelle and the ER and the functional importance of these small specialized membrane domains is increasingly recognized...
December 6, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/29188077/orai1-2-3-and-stim1-promote-store-operated-calcium-entry-in-pulmonary-arterial-smooth-muscle-cells
#14
Jian Wang, Chuyi Xu, Qiuyu Zheng, Kai Yang, Ning Lai, Tao Wang, Haiyang Tang, Wenju Lu
Previous studies have demonstrated that besides the classic canonical transient receptor potential channel family, Orai family and stromal interaction molecule 1 (STIM1) might also be involved in the regulation of store-operated calcium channels (SOCCs). An increase in cytosolic free Ca2+ concentration promoted by store-operated Ca2+ entry (SOCE) in pulmonary arterial smooth muscle cells (PASMCs) is a major trigger for pulmonary vasoconstriction and proliferation and migration of PASMCs. In this study, our data revealed the following: (1) in both rat distal pulmonary arteries and PASMCs, chronic hypoxia exposure upregulated the expression of Orai1 and Orai2, without affecting Orai3 and STIM1; (2) either heterozygous knockout of HIF-1α in mice or knockdown of HIF-1α in PASMCs abolished the hypoxic upregulation of Orai2, but not Orai1, suggesting the hypoxic upregulation of Orai2 depends on HIF-1α; and (3) using small interference RNA knockdown strategies, Orai1, 2, 3 and STIM1 were all shown to mediate SOCE in hypoxic PASMCs...
2017: Cell Death Discovery
https://www.readbyqxmd.com/read/29184418/fgf2-promotes-metastasis-of-uveal-melanoma-cells-via-store-operated-calcium-entry
#15
Yanyan Wang, Xiuli Bao, Zhiyong Zhang, Yi Sun, Xiyuan Zhou
Uveal melanoma (UM), the most common primary intraocular malignancy in adults, is highly metastatic and associated with dismal prognosis. Fibroblast growth factor 2 (FGF2) has been shown to induce cell proliferation and angiogenesis of melanoma and other malignancies. However, the expression of FGF2 in UM and its effects on melanoma cell migration are not well known. In this study, we found FGF2 expression was related to UM histological subtype and presence of metastasis. In vitro experiments showed that FGF2 treatment caused increased horizontal and vertical migration and F-actin cytoskeleton assembly as well as decreased adhesive activity of MUM2B cells, together with increased intracellular calcium concentration and expression of ORAI1 and STIM1 - two key regulatory proteins of store-operated calcium entry (SOCE)...
2017: OncoTargets and Therapy
https://www.readbyqxmd.com/read/29179176/neurons-erythrocytes-and-beyond-the-diverse-functions-of-chorein
#16
Florian Lang, Lisann Pelzl, Ludger Schöls, Andreas Hermann, Michael Föller, Tilman E Schäffer, Christos Stournaras
Chorea-acanthocytosis (ChAc), a neurodegenerative disease, results from loss-of-function-mutations of the chorein-encoding gene VPS13A. Affected patients suffer from a progressive movement disorder including chorea, parkinsonism, dystonia, tongue protrusion, dysarthria, dysphagia, tongue and lip biting, gait impairment, progressive distal muscle wasting, weakness, epileptic seizures, cognitive impairment, and behavioral changes. Those pathologies may be paralleled by erythrocyte acanthocytosis. Chorein supports activation of phosphoinositide-3-kinase (PI3K)-p85-subunit with subsequent up-regulation of ras-related C3 botulinum toxin substrate 1 (Rac1) activity, p21 protein-activated kinase 1 (PAK1) phosphorylation, and activation of several tyrosine kinases...
November 28, 2017: Neuro-Signals
https://www.readbyqxmd.com/read/29167149/three-dimensional-imaging-reveals-endo-sarco-plasmic-reticulum-containing-invaginations-within-the-muscle-nucleoplasm
#17
Shin-Haw Lee, Sina Hadipour-Lakmehsari, Tetsuaki Miyake, Anthony O Gramolini
The mammalian nucleus has invaginations from the cytoplasm, termed nucleoplasmic reticulum (NR). With increased resolution of cellular imaging, progress has been made in understanding the formation and function of NR. In fact, nucleoplasmic Ca2+ homeostasis has been implicated in the regulation of gene expression, DNA repair, and cell death. However, the majority of studies focus on cross-sectional or single plane analyses of NR invaginations, providing an incomplete assessment of its distribution and content...
November 22, 2017: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/29163766/epigallocatechin-3-gallate-egcg-up-regulates-mir-15b-expression-thus-attenuating-store-operated-calcium-entry-soce-into-murine-cd4-t-cells-and-human-leukaemic-t-cell-lymphoblasts
#18
Shaqiu Zhang, Tamer Al-Maghout, Rosi Bissinger, Ni Zeng, Lisann Pelzl, Madhuri S Salker, Anchun Cheng, Yogesh Singh, Florian Lang
CD4(+) T cells are key elements in immune responses and inflammation. Activation of T cell receptors in CD4(+) T cells triggers cytosolic Ca(2+) release with subsequent store operated Ca(2+) entry (SOCE), which is accomplished by the pore forming Ca(2+) release activated Ca(2+) (CRAC) channel Orai1 and its regulator stromal cell-interaction molecule 2 (STIM2). Green tea polyphenol epigallocatechin-3-gallate (EGCG) acts as a potent anti-inflammatory and anti-oxidant agent for various types of cells including immune cells...
October 27, 2017: Oncotarget
https://www.readbyqxmd.com/read/29155098/orai1-mutations-abolishing-store-operated-ca-2-entry-cause-anhidrotic-ectodermal-dysplasia-with-immunodeficiency-eda-id
#19
Jayson Lian, Mario Cuk, Sascha Kahlfuss, Lina Kozhaya, Martin Vaeth, Frédéric Rieux-Laucat, Capucine Picard, Melina J Benson, Antonia Jakovcevic, Karmen Bilic, Iva Martinac, Peter Stathopulos, Imre Kacskovics, Thomas Vraetz, Carsten Speckmann, Stephan Ehl, Thomas Issekutz, Derya Unutmaz, Stefan Feske
BACKGROUND: Store-operated Ca(2+) entry (SOCE) through Ca(2+) release-activated Ca(2+) (CRAC) channels is an essential signaling pathway in many cell types. CRAC channels are formed by ORAI1, ORAI2 and ORAI3 proteins and activated by stromal interaction molecule 1 (STIM1) and STIM2. Mutations in ORAI1 and STIM1 genes that abolish SOCE cause a combined immunodeficiency (CID) syndrome that is accompanied by autoimmunity and non-immunological symptoms. OBJECTIVE: Molecular and immunological analysis of patients with CID, anhidrosis and ectodermal dysplasia of unknown etiology...
November 15, 2017: Journal of Allergy and Clinical Immunology
https://www.readbyqxmd.com/read/29129621/tdcpp-protects-cardiomyocytes-from-hypoxia-reoxygenation-injury-induced-apoptosis-through-mitigating-calcium-overload-and-promotion-gsk-3%C3%AE-phosphorylation
#20
Xiju He, Shoutian Li, Xiaoxia Fang, Yanhong Liao
TDCPP, Tris (1, 3-dichloro-2-propyl) phosphate belongs to a group of chemicals known as triester organophosphate flame retardants, It can alter calcium homeostasis at much lower concentrations in normal conditions, but the mechanism is unclear till now. Calcium overload is a leading cause of apoptosis in myocardial ischemia/reperfusion (I/R) injury, thus how to mitigate Ca(2+)-overload is deserved to be investigated. We therefore hypothesized that TDCPP could attenuate cardiomyocytes apoptosis in I/R injury...
November 9, 2017: Regulatory Toxicology and Pharmacology: RTP
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