Base de dados : MEDLINE
Pesquisa : D12.776.157.125.806.750 [Categoria DeCS]
Referências encontradas : 131 [refinar]
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  1 / 131 MEDLINE  
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[PMID]:29030115
[Au] Autor:Vaeth M; Maus M; Klein-Hessling S; Freinkman E; Yang J; Eckstein M; Cameron S; Turvey SE; Serfling E; Berberich-Siebelt F; Possemato R; Feske S
[Ad] Endereço:Department of Pathology, New York University School of Medicine, New York, NY 10016, USA.
[Ti] Título:Store-Operated Ca Entry Controls Clonal Expansion of T Cells through Metabolic Reprogramming.
[So] Source:Immunity;47(4):664-679.e6, 2017 Oct 17.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Store-operated Ca entry (SOCE) is the main Ca influx pathway in lymphocytes and is essential for T cell function and adaptive immunity. SOCE is mediated by Ca release-activated Ca (CRAC) channels that are activated by stromal interaction molecule (STIM) 1 and STIM2. SOCE regulates many Ca -dependent signaling molecules, including calcineurin, and inhibition of SOCE or calcineurin impairs antigen-dependent T cell proliferation. We here report that SOCE and calcineurin regulate cell cycle entry of quiescent T cells by controlling glycolysis and oxidative phosphorylation. SOCE directs the metabolic reprogramming of naive T cells by regulating the expression of glucose transporters, glycolytic enzymes, and metabolic regulators through the activation of nuclear factor of activated T cells (NFAT) and the PI3K-AKT kinase-mTOR nutrient-sensing pathway. We propose that SOCE controls a critical "metabolic checkpoint" at which T cells assess adequate nutrient supply to support clonal expansion and adaptive immune responses.
[Mh] Termos MeSH primário: Canais de Cálcio/imunologia
Sinalização do Cálcio/imunologia
Cálcio/imunologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Calcineurina/imunologia
Calcineurina/metabolismo
Cálcio/metabolismo
Canais de Cálcio/metabolismo
Divisão Celular/imunologia
Células Cultivadas
Feminino
Glicólise/imunologia
Células HEK293
Seres Humanos
Immunoblotting
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Microscopia Confocal
Fatores de Transcrição NFATC/genética
Fatores de Transcrição NFATC/imunologia
Fatores de Transcrição NFATC/metabolismo
Fosfatidilinositol 3-Quinases/imunologia
Fosfatidilinositol 3-Quinases/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais/imunologia
Molécula 1 de Interação Estromal/genética
Molécula 1 de Interação Estromal/imunologia
Molécula 1 de Interação Estromal/metabolismo
Molécula 2 de Interação Estromal/genética
Molécula 2 de Interação Estromal/imunologia
Molécula 2 de Interação Estromal/metabolismo
Linfócitos T/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels); 0 (NFATC Transcription Factors); 0 (Stromal Interaction Molecule 1); 0 (Stromal Interaction Molecule 2); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 3.1.3.16 (Calcineurin); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171015
[St] Status:MEDLINE


  2 / 131 MEDLINE  
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[PMID]:28724541
[Au] Autor:Clemens RA; Chong J; Grimes D; Hu Y; Lowell CA
[Ad] Endereço:Department of Pediatrics, University of California, San Francisco, CA.
[Ti] Título:STIM1 and STIM2 cooperatively regulate mouse neutrophil store-operated calcium entry and cytokine production.
[So] Source:Blood;130(13):1565-1577, 2017 Sep 28.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neutrophils are key effector cells of the innate immune system. Calcium-dependent signaling pathways initiated by store-operated calcium entry (SOCE) are known to regulate neutrophil activation; however, the precise mechanism of this process remains unclear. STIM1 and STIM2 are calcium-sensing molecules that link calcium depletion of the endoplasmic reticulum with opening of plasma membrane calcium channels. Although a role for STIM1 in neutrophil SOCE and activation has been established, the function of STIM2 is unknown. Here we use mice with conditional ablation of and/or to investigate the role of STIM2 in neutrophil activation. We demonstrate that loss of STIM2 results in decreased SOCE, particularly at lower doses of agonists. Reactive oxygen species (ROS) production, degranulation, and phagocytosis are normal in the absence of STIM2, suggesting STIM1 is the dominant calcium sensor required for classical short-term neutrophil responses. However, neutrophil cytokine production required STIM2, but not STIM1, at least in part as a result of redox regulation of cytokine gene expression. In vivo loss of STIM2 results in lower cytokine levels and protection from mortality in a mouse model of systemic inflammatory response syndrome. These data, combined with previous studies focusing on STIM1, define distinct but cooperative functions for STIM1 and STIM2 in modulating neutrophil bactericidal and cytokine responses.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Citocinas/biossíntese
Ativação de Neutrófilo
Molécula 1 de Interação Estromal/fisiologia
Molécula 2 de Interação Estromal/fisiologia
[Mh] Termos MeSH secundário: Animais
Canais de Cálcio/metabolismo
Camundongos
Oxirredução
Molécula 1 de Interação Estromal/imunologia
Molécula 2 de Interação Estromal/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels); 0 (Cytokines); 0 (Stim1 protein, mouse); 0 (Stim2 protein, mouse); 0 (Stromal Interaction Molecule 1); 0 (Stromal Interaction Molecule 2); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2016-11-751230


  3 / 131 MEDLINE  
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[PMID]:28479254
[Au] Autor:Zhang S; Miao Y; Zheng X; Gong Y; Zhang J; Zou F; Cai C
[Ad] Endereço:Department of Occupational Health and Occupational Medicine, School of Public Health, Southern Medical University, Guangzhou, Guangdong 510515, China; People's Hospital of Bao'an, Shenzhen, Guangdong 518101, China.
[Ti] Título:STIM1 and STIM2 differently regulate endogenous Ca entry and promote TGF-ß-induced EMT in breast cancer cells.
[So] Source:Biochem Biophys Res Commun;488(1):74-80, 2017 Jun 17.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The Ca sensor proteins STIM1 and STIM2 are crucial elements of store-operated calcium entry (SOCE) in breast cancer cells. Increased SOCE activity may contribute to epithelial-mesenchymal transitions (EMT) and increase cell migration and invasion. However, the roles of STIM1 and STIM2 in TGF-ß-induced EMT are still unclear. In this study, we demonstrate roles of STIMs in TGF-ß-induced EMT in breast cancer cells. In particular, STIM1 and STIM2 expression affected TGF-ß-induced EMT by mediating SOCE in MDA-MB-231 and MCF-7 breast cancer cells. The specific SOCE inhibitor YM58483 blocked TGF-ß-induced EMT, and differing effects of STIM1 and STIM2 on TGF-ß-induced EMT correlated with differing roles in SOCE. Finally, we showed that STIM2 is associated with non-store-operated calcium entry (non-SOCE) during TGF-ß-induced EMT, whereas STIM1 is not. What's more, non-SOCE have a large possibility to be ROCE. In conclusion, STIM1 and STIM2 proteins play important roles in TGF-ß-induced EMT and these effects are related to both SOCE and non-SOCE.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Cálcio/metabolismo
Transição Epitelial-Mesenquimal
Proteínas de Neoplasias/metabolismo
Molécula 1 de Interação Estromal/metabolismo
Molécula 2 de Interação Estromal/metabolismo
Fator de Crescimento Transformador beta/metabolismo
[Mh] Termos MeSH secundário: Neoplasias da Mama/patologia
Seres Humanos
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neoplasm Proteins); 0 (STIM1 protein, human); 0 (STIM2 protein, human); 0 (Stromal Interaction Molecule 1); 0 (Stromal Interaction Molecule 2); 0 (Transforming Growth Factor beta); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE


  4 / 131 MEDLINE  
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[PMID]:28446591
[Au] Autor:Sahu I; Pelzl L; Sukkar B; Fakhri H; Al-Maghout T; Cao H; Hauser S; Gutti R; Gawaz M; Lang F
[Ad] Endereço:Department of Cardiology and Vascular Medicine and Physiology, University of Tübingen, Tübingen, Germany.
[Ti] Título:NFAT5-sensitive Orai1 expression and store-operated Ca entry in megakaryocytes.
[So] Source:FASEB J;31(8):3439-3448, 2017 Aug.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The transcription factor nuclear factor of activated T cells 5 (NFAT5) is up-regulated in several clinical disorders, including dehydration. NFAT5-sensitive genes include serum and glucocorticoid-inducible kinase 1 (SGK1). The kinase is a powerful regulator of Orai1, a Ca channel accomplishing store-operated Ca entry (SOCE). Orai1 is stimulated after intracellular store depletion by the Ca sensors stromal interaction molecule 1 (STIM1), or STIM2, or both. In the present study, we explored whether nuclear factor of activated T cell (NFAT)-5 influences Ca signaling in megakaryocytes. To this end, human megakaryocytic (MEG-01) cells were transfected with NFAT5 or with siNFAT5. Platelets and megakaryocytes were isolated from wild-type mice with either access to water or dehydration by 36 h of water deprivation. Transcript levels were determined with quantitative RT-PCR and protein abundance by Western blot analysis and flow cytometry, cytosolic (intracellular) Ca concentration ([Ca ] ) by fura-2-fluorescence. SOCE was estimated from the increase of [Ca ] following readdition of extracellular Ca after store depletion with thapsigargin (1 µM). Platelet degranulation was estimated from P-selectin abundance and integrin activation from α ß integrin abundance determined by flow cytometry. As a result, NFAT5 transfection or exposure to hypertonicity (+40 mM NaCl) of MEG-01 cells increased Orai1, Orai2, STIM1, and STIM2 transcript levels. Orai1 transcript levels were decreased by NFAT5 silencing. NFAT5 transfection and IκB inhibitor BMS 345541 (5 µM) increased SOCE, whereas NFAT5 silencing and SGK1 inhibitor GSK650394 (10 µM) decreased SOCE. In the mice, dehydration increased NFAT5 and Orai1 protein abundance in megakaryocytes and NFAT5, Orai1, and Orai2 abundance in platelets. Dehydration further augmented the degranulation and integrin activation by thrombin and collagen-related peptide. In summary, NFAT5 is a powerful regulator of Orai1-expression and SOCE in megakaryocytes.-Sahu, I., Pelzl, L., Sukkar, B., Fakhri, H., al-Maghout, T., Cao, H., Hauser, S., Gutti, R., Gawaz, M., Lang, F. NFAT5-sensitive Orai1 expression and store-operated Ca entry in megakaryocytes.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Megacariócitos/metabolismo
Proteína ORAI1/metabolismo
Proteína ORAI2/metabolismo
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Animais
Plaquetas
Linhagem Celular
Feminino
Regulação da Expressão Gênica/fisiologia
Seres Humanos
Masculino
Camundongos
Proteína ORAI1/genética
Proteína ORAI2/genética
Molécula 1 de Interação Estromal/genética
Molécula 1 de Interação Estromal/metabolismo
Molécula 2 de Interação Estromal/genética
Molécula 2 de Interação Estromal/metabolismo
Fatores de Transcrição/genética
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nfat5 protein, mouse); 0 (ORAI1 Protein); 0 (ORAI2 Protein); 0 (Orai1 protein, mouse); 0 (Orai2 protein, mouse); 0 (Stim1 protein, mouse); 0 (Stim2 protein, mouse); 0 (Stromal Interaction Molecule 1); 0 (Stromal Interaction Molecule 2); 0 (Transcription Factors); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1096/fj.201601211R


  5 / 131 MEDLINE  
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[PMID]:27721237
[Au] Autor:Concepcion AR; Vaeth M; Wagner LE; Eckstein M; Hecht L; Yang J; Crottes D; Seidl M; Shin HP; Weidinger C; Cameron S; Turvey SE; Issekutz T; Meyts I; Lacruz RS; Cuk M; Yule DI; Feske S
[Ti] Título:Store-operated Ca2+ entry regulates Ca2+-activated chloride channels and eccrine sweat gland function.
[So] Source:J Clin Invest;126(11):4303-4318, 2016 Nov 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo: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. SOCE was absent in agonist-stimulated sweat glands from Orai1K14Cre and Stim1/2K14Cre mice and human sweat gland cells lacking ORAI1 or STIM1 expression. In Orai1K14Cre mice, abolishment of SOCE was associated with impaired chloride secretion by primary murine sweat glands. In human sweat gland cells, SOCE mediated by ORAI1 was necessary for agonist-induced chloride secretion and activation of the Ca2+-activated chloride channel (CaCC) anoctamin 1 (ANO1, also known as TMEM16A). By contrast, expression of TMEM16A, the water channel aquaporin 5 (AQP5), and other regulators of sweat gland function was normal in the absence of SOCE. Our findings demonstrate that Ca2+ influx via store-operated CRAC channels is essential for CaCC activation, chloride secretion, and sweat production in humans and mice.
[Mh] Termos MeSH primário: Sinalização do Cálcio/fisiologia
Canais de Cloreto/metabolismo
Proteínas de Neoplasias/metabolismo
Proteína ORAI1/metabolismo
Glândulas Sudoríparas/metabolismo
Suor/secreção
[Mh] Termos MeSH secundário: Animais
Anoctamina-1
Aquaporina 5/genética
Aquaporina 5/metabolismo
Canais de Cloreto/genética
Feminino
Seres Humanos
Masculino
Camundongos
Camundongos Knockout
Proteínas de Neoplasias/genética
Proteína ORAI1/genética
Molécula 1 de Interação Estromal/genética
Molécula 1 de Interação Estromal/metabolismo
Molécula 2 de Interação Estromal/genética
Molécula 2 de Interação Estromal/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ANO1 protein, human); 0 (ANO1 protein, mouse); 0 (AQP5 protein, human); 0 (Anoctamin-1); 0 (Aqp5 protein, mouse); 0 (Aquaporin 5); 0 (Chloride Channels); 0 (Neoplasm Proteins); 0 (ORAI1 Protein); 0 (ORAI1 protein, human); 0 (Orai1 protein, mouse); 0 (STIM1 protein, human); 0 (STIM2 protein, human); 0 (Stim1 protein, mouse); 0 (Stim2 protein, mouse); 0 (Stromal Interaction Molecule 1); 0 (Stromal Interaction Molecule 2)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161011
[St] Status:MEDLINE


  6 / 131 MEDLINE  
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[PMID]:27261277
[Au] Autor:Vaeth M; Eckstein M; Shaw PJ; Kozhaya L; Yang J; Berberich-Siebelt F; Clancy R; Unutmaz D; Feske S
[Ad] Endereço:Department of Pathology, New York University School of Medicine, New York, NY 10016, USA.
[Ti] Título:Store-Operated Ca(2+) Entry in Follicular T Cells Controls Humoral Immune Responses and Autoimmunity.
[So] Source:Immunity;44(6):1350-64, 2016 06 21.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:T follicular helper (Tfh) cells promote affinity maturation of B cells in germinal centers (GCs), whereas T follicular regulatory (Tfr) cells limit the GC reaction. Store-operated Ca(2+) entry (SOCE) through Ca(2+) release-activated Ca(2+) (CRAC) channels mediated by STIM and ORAI proteins is a fundamental signaling pathway in T lymphocytes. Conditional deletion of Stim1 and Stim2 genes in T cells abolished SOCE and strongly reduced antibody-mediated immune responses following viral infection caused by impaired differentiation and function of Tfh cells. Conversely, aging Stim1Stim2-deficient mice developed humoral autoimmunity with spontaneous autoantibody production due to abolished Tfr cell differentiation in the presence of residual Tfh cells. Mechanistically, SOCE controlled Tfr and Tfh cell differentiation through NFAT-mediated IRF4, BATF, and Bcl-6 transcription-factor expression. SOCE had a dual role in controlling the GC reaction by regulating both Tfh and Tfr cell differentiation, thus enabling protective B cell responses and preventing humoral autoimmunity.
[Mh] Termos MeSH primário: Autoimunidade
Linfócitos B/imunologia
Centro Germinativo/imunologia
Imunidade Humoral
Molécula 1 de Interação Estromal/metabolismo
Molécula 2 de Interação Estromal/metabolismo
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Fatores de Transcrição de Zíper de Leucina Básica/genética
Fatores de Transcrição de Zíper de Leucina Básica/metabolismo
Canais de Cálcio Ativados pela Liberação de Cálcio/metabolismo
Sinalização do Cálcio
Células Cultivadas
Fatores Reguladores de Interferon/genética
Fatores Reguladores de Interferon/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fatores de Transcrição NFATC/metabolismo
Proteína ORAI1/metabolismo
Proteínas Proto-Oncogênicas c-bcl-6/genética
Proteínas Proto-Oncogênicas c-bcl-6/metabolismo
Molécula 1 de Interação Estromal/genética
Molécula 2 de Interação Estromal/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Basic-Leucine Zipper Transcription Factors); 0 (Batf protein, mouse); 0 (Bcl6 protein, mouse); 0 (Calcium Release Activated Calcium Channels); 0 (Interferon Regulatory Factors); 0 (NFATC Transcription Factors); 0 (ORAI1 Protein); 0 (Orai1 protein, mouse); 0 (Proto-Oncogene Proteins c-bcl-6); 0 (Stromal Interaction Molecule 1); 0 (Stromal Interaction Molecule 2); 0 (interferon regulatory factor-4)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171119
[Lr] Data última revisão:
171119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160605
[St] Status:MEDLINE


  7 / 131 MEDLINE  
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[PMID]:27245842
[Au] Autor:Gao X; Xia J; Munoz FM; Manners MT; Pan R; Meucci O; Dai Y; Hu H
[Ad] Endereço:Department of Pharmacology and Physiology, Drexel University College of Medicine, 245 N. 15th Street, Philadelphia, PA, 19102, USA.
[Ti] Título:STIMs and Orai1 regulate cytokine production in spinal astrocytes.
[So] Source:J Neuroinflammation;13(1):126, 2016 May 31.
[Is] ISSN:1742-2094
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Our previous study demonstrated that a store-operated calcium channel (SOCC) inhibitor (YM-58483) has central analgesic effects. However, the cellular and molecular mechanisms of such effects remain to be determined. It is well-known that glial cells play important roles in central sensitization. SOC entry (SOCE) has been implicated in many cell types including cortical astrocytes. However, the role of the SOCC family in the function of astrocytes has not been determined. Here, we thoroughly investigated the expression and the functional significance of SOCCs in spinal astrocytes. METHODS: Primary cultured astrocytes were prepared from neonatal (P2-P3) CD1 mice. Expressions of mRNAs and proteins were respectively assessed by real-time PCR and Western blot analysis. SOCE was measured using a calcium imaging system. Live-cell STIM1 translocation was detected using a confocal microscope. Cytokine levels were measured by the enzyme-linked immunosorbent assay. RESULTS: We found that the SOCC family is expressed in spinal astrocytes and that depletion of calcium stores from the endoplasmic reticulum by cyclopiazonic acid (CPA) resulted in a large sustained calcium entry, which was blocked by SOCC inhibitors. Using the siRNA knockdown approach, we identified STIM1 and Orai1 as primary components of SOCCs in spinal astrocytes. We also observed thapsigargin (TG)- or CPA-induced puncta formation of STIM1 and Orai1. In addition, activation of SOCCs remarkably promoted TNF-α and IL-6 production in spinal astrocytes, which were greatly attenuated by knockdown of STIM1 or Orai1. Importantly, knockdown of STIM2 and Orai1 dramatically decreased lipopolysaccharide-induced TNF-α and IL-6 production without changing cell viability. CONCLUSIONS: This study presents the first evidence that STIM1, STIM2, and Orai1 mediate SOCE and are involved in cytokine production in spinal astrocytes. Our findings provide the basis for future assessment of SOCCs in pain and other central nervous system disorders associated with abnormal astrocyte activities.
[Mh] Termos MeSH primário: Astrócitos/metabolismo
Citocinas/biossíntese
Proteína ORAI1/fisiologia
Medula Espinal/metabolismo
Molécula 1 de Interação Estromal/fisiologia
Molécula 2 de Interação Estromal/fisiologia
[Mh] Termos MeSH secundário: Anilidas/farmacologia
Animais
Animais Recém-Nascidos
Astrócitos/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/fisiologia
Células Cultivadas
Feminino
Camundongos
Proteína ORAI1/antagonistas & inibidores
Gravidez
Medula Espinal/efeitos dos fármacos
Molécula 1 de Interação Estromal/antagonistas & inibidores
Molécula 2 de Interação Estromal/antagonistas & inibidores
Tiadiazóis/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-methyl-4'-(3,5-bis(trifluoromethyl)-1H-pyrazol-1-yl)-1,2,3-thiadiazole-5-carboxanilide); 0 (Anilides); 0 (Cytokines); 0 (ORAI1 Protein); 0 (Orai1 protein, mouse); 0 (Stim1 protein, mouse); 0 (Stim2 protein, mouse); 0 (Stromal Interaction Molecule 1); 0 (Stromal Interaction Molecule 2); 0 (Thiadiazoles)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160602
[St] Status:MEDLINE
[do] DOI:10.1186/s12974-016-0594-7


  8 / 131 MEDLINE  
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[PMID]:27161226
[Au] Autor:Ong HL; de Souza LB; Ambudkar IS
[Ad] Endereço:Secretory Physiology Section, Molecular Physiology and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Building 10, Room 1N-113, NIH, Bethesda, MD, 20892, USA. ongh@mail.nih.gov.
[Ti] Título:Role of TRPC Channels in Store-Operated Calcium Entry.
[So] Source:Adv Exp Med Biol;898:87-109, 2016.
[Is] ISSN:0065-2598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Store-operated calcium entry (SOCE) is a ubiquitous Ca(2+) entry pathway that is activated in response to depletion of Ca(2+) stores within the endoplasmic reticulum (ER) and contributes to the control of various physiological functions in a wide variety of cell types. The transient receptor potential canonical (TRPC) channels (TRPCs 1-7), that are activated by stimuli leading to PIP2 hydrolysis, were first identified as molecular components of SOCE channels. TRPC channels show a miscellany of tissue expression, physiological functions and channel properties. However, none of the TRPC members display currents that resemble I CRAC. Intensive search for the CRAC channel component led to identification of Orai1 and STIM1, now established as being the primary constituents of the CRAC channel. There is now considerable evidence that STIM1 activates both Orai1 and TRPC1 via distinct domains in its C-terminus. Intriguingly, TRPC1 function is not only dependent on STIM1 but also requires Orai1. The critical functional interaction between TRPC1 and Orai1, which determines the activation of TRPC1, has also been identified. In this review, we will discuss current concepts regarding the role of TRPC channels in SOCE, the physiological functions regulated by TRPC-mediated SOCE, and the complex mechanisms underlying the regulation of TRPCs, including the functional interactions with Orai1 and STIM1.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Canais de Cátion TRPC/fisiologia
[Mh] Termos MeSH secundário: Moléculas de Adesão Celular/metabolismo
Seres Humanos
Transporte de Íons
Proteínas de Membrana/metabolismo
Proteínas de Neoplasias/metabolismo
Molécula 1 de Interação Estromal
Molécula 2 de Interação Estromal
Canais de Cátion TRPC/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., INTRAMURAL; REVIEW
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (Membrane Proteins); 0 (Neoplasm Proteins); 0 (STIM1 protein, human); 0 (STIM2 protein, human); 0 (Stromal Interaction Molecule 1); 0 (Stromal Interaction Molecule 2); 0 (TRPC Cation Channels); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160511
[St] Status:MEDLINE
[do] DOI:10.1007/978-3-319-26974-0_5


  9 / 131 MEDLINE  
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[PMID]:26985029
[Au] Autor:Molnár T; Yarishkin O; Iuso A; Barabas P; Jones B; Marc RE; Phuong TT; Krizaj D
[Ad] Endereço:Departments of Ophthalmology & Visual Sciences.
[Ti] Título:Store-Operated Calcium Entry in Müller Glia Is Controlled by Synergistic Activation of TRPC and Orai Channels.
[So] Source:J Neurosci;36(11):3184-98, 2016 Mar 16.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: The endoplasmic reticulum (ER) is at the epicenter of astrocyte Ca(2+) signaling. We sought to identify the molecular mechanism underlying store-operated calcium entry that replenishes ER stores in mouse Müller cells. Store depletion, induced through blockade of sequestration transporters in Ca(2+)-free saline, induced synergistic activation of canonical transient receptor potential 1 (TRPC1) and Orai channels. Store-operated TRPC1 channels were identified by their electrophysiological properties, pharmacological blockers, and ablation of the Trpc1 gene. Ca(2+) release-activated currents (ICRAC) were identified by ion permeability, voltage dependence, and sensitivity to selective Orai antagonists Synta66 and GSK7975A. Depletion-evoked calcium influx was initiated at the Müller end-foot and apical process, triggering centrifugal propagation of Ca(2+) waves into the cell body. EM analysis of the end-foot compartment showed high-density ER cisternae that shadow retinal ganglion cell (RGC) somata and axons, protoplasmic astrocytes, vascular endothelial cells, and ER-mitochondrial contacts at the vitreal surface of the end-foot. The mouse retina expresses transcripts encoding both Stim and all known Orai genes; Müller glia predominantly express stromal interacting molecule 1 (STIM1), whereas STIM2 is mainly confined to the outer plexiform and RGC layers. Elimination of TRPC1 facilitated Müller gliosis induced by the elevation of intraocular pressure, suggesting that TRPC channels might play a neuroprotective role during mechanical stress. By characterizing the properties of store-operated signaling pathways in Müller cells, these studies expand the current knowledge about the functional roles these cells play in retinal physiology and pathology while also providing further evidence for the complexity of calcium signaling mechanisms in CNS astroglia. SIGNIFICANCE STATEMENT: Store-operated Ca(2+) signaling represents a major signaling pathway and source of cytosolic Ca(2+) in astrocytes. Here, we show that the store-operated response in Müller cells, radial glia that perform key structural, signaling, osmoregulatory, and mechanosensory functions within the retina, is mediated through synergistic activation of transient receptor potential and Orai channels. The end-foot disproportionately expresses the depletion sensor stromal interacting molecule 1, which contains an extraordinarily high density of endoplasmic reticulum cisternae that shadow neuronal, astrocytic, vascular, and axonal structures; interface with mitochondria; but also originate store-operated Ca(2+) entry-induced transcellular Ca(2+) waves that propagate glial excitation into the proximal retina. These results identify a molecular mechanism that underlies complex interactions between the plasma membrane and calcium stores, and contributes to astroglial function, regulation, and response to mechanical stress.
[Mh] Termos MeSH primário: Canais de Cálcio/metabolismo
Cálcio/metabolismo
Células Ependimogliais/metabolismo
Canais de Cátion TRPC/metabolismo
[Mh] Termos MeSH secundário: Animais
Benzamidas/farmacologia
Bloqueadores dos Canais de Cálcio/farmacologia
Canais de Cálcio/genética
Modelos Animais de Doenças
Retículo Endoplasmático/metabolismo
Células Ependimogliais/efeitos dos fármacos
Células Ependimogliais/ultraestrutura
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/genética
Proteína Glial Fibrilar Ácida/metabolismo
Masculino
Glicoproteínas de Membrana/metabolismo
Potenciais da Membrana/efeitos dos fármacos
Potenciais da Membrana/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Hipertensão Ocular/induzido quimicamente
Hipertensão Ocular/patologia
Pirazóis/farmacologia
Retina/citologia
Molécula 1 de Interação Estromal
Molécula 2 de Interação Estromal
Canais de Cátion TRPC/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; VIDEO-AUDIO MEDIA
[Nm] Nome de substância:
0 (2,6-difluoro-N-(1-(4-hydroxy-2-(trifluoromethyl)benzyl)-1H-pyrazol-3-yl)benzamide); 0 (Benzamides); 0 (Calcium Channel Blockers); 0 (Calcium Channels); 0 (Glial Fibrillary Acidic Protein); 0 (Membrane Glycoproteins); 0 (Pyrazoles); 0 (Stim1 protein, mouse); 0 (Stim2 protein, mouse); 0 (Stromal Interaction Molecule 1); 0 (Stromal Interaction Molecule 2); 0 (TRPC Cation Channels); 0 (Trpc2 protein, mouse); 0 (transient receptor potential cation channel, subfamily C, member 1); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160318
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.4069-15.2016


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[PMID]:26960935
[Au] Autor:Kuang XL; Liu Y; Chang Y; Zhou J; Zhang H; Li Y; Qu J; Wu S
[Ad] Endereço:School of Optometry and Ophthalmology and the Eye Hospital, Wenzhou Medical University, 270 Xueyuan Road, Wenzhou, Zhejiang 325003, PR China; Cultivation Base and Key Laboratory of Vision Science, Ministry of Health and Zhejiang Provincial Key Laboratory of Ophthalmology and Optometry, Wenzhou Medic
[Ti] Título:Inhibition of store-operated calcium entry by sub-lethal levels of proteasome inhibition is associated with STIM1/STIM2 degradation.
[So] Source:Cell Calcium;59(4):172-80, 2016 04.
[Is] ISSN:1532-1991
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Dysfunction of the ubiquitin-proteasome system (UPS) and calcium homeostasis has been implicated in the neurodegeneration of Alzheimer's and Parkinson's diseases. The cytosolic calcium concentration is maintained by store-operated calcium entry (SOCE), which is repressed by Alzheimer's disease-associated mutants, such as mutant presenilins. We hypothesized that inhibition of UPS impacts SOCE. This study showed that pretreatment with sub-lethal levels of proteasome inhibitors, including MG-132 and clasto-lactacystin-ß-lactone (LA), reduced SOCE after depletion of endoplasmic reticulum calcium in rat neurons. With the same treatment, MG-132 and LA reduced the protein levels of stromal interaction molecule 1and 2 (STIM1/2), but not the levels of Orai1 and canonical transient receptor potential channel 1 (TRPC1). STIM1 or STIM2 protein was mobilized to lysosome by MG-132/LA treatment as observed under an immunofluorescence confocal laser microscope. In the neurons, MG-132 and LA degraded p62/SQSTM1, promoted autophagy, converted LC3I to LC3II, and promoted co-localization of LC3 and lysosomes. Rapamycin, which enhances autophagy, reduced STIM1/2 protein levels, whereas bafilomycin, which inhibits autophagy, increased their protein levels. The protein levels of STIM1/2 and the amplitude of SOCE were decreased in SH-SY5Y with decreased protein level of proteasome subunit beta type-5 induced by shRNA. We conclude that sub-lethal levels of proteasome inhibition reduce SOCE and promote autophagy-mediated degradation of STIM1/2. UPS inhibition, a common finding in neurodegenerative diseases, interferes with calcium homeostasis via repression of SOCE.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Complexo de Endopeptidases do Proteassoma/efeitos adversos
Molécula 1 de Interação Estromal/metabolismo
Molécula 2 de Interação Estromal/metabolismo
[Mh] Termos MeSH secundário: Animais
Canais de Cálcio/metabolismo
Retículo Endoplasmático/metabolismo
Transporte de Íons/fisiologia
Glicoproteínas de Membrana/metabolismo
Proteínas de Membrana/metabolismo
Neurônios/metabolismo
Complexo de Endopeptidases do Proteassoma/metabolismo
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Calcium Channels); 0 (Membrane Glycoproteins); 0 (Membrane Proteins); 0 (STIM2 protein, rat); 0 (Stim1 protein, rat); 0 (Stromal Interaction Molecule 1); 0 (Stromal Interaction Molecule 2); EC 3.4.25.1 (Proteasome Endopeptidase Complex); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170222
[Lr] Data última revisão:
170222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160311
[St] Status:MEDLINE



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