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Pesquisa : D12.776.395.550.200.537.937 [Categoria DeCS]
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  1 / 6 MEDLINE  
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[PMID]:28196865
[Au] Autor:Aramsangtienchai P; Spiegelman NA; Cao J; Lin H
[Ad] Endereço:From the Howard Hughes Medical Institute, Department of Chemistry and Chemical Biology, Cornell University, Ithaca, New York 14853.
[Ti] Título:-Palmitoylation of Junctional Adhesion Molecule C Regulates Its Tight Junction Localization and Cell Migration.
[So] Source:J Biol Chem;292(13):5325-5334, 2017 Mar 31.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Junctional adhesion molecule C (JAM-C) is an immunoglobulin superfamily protein expressed in epithelial cells, endothelial cells, and leukocytes. JAM-C has been implicated in leukocyte transendothelial migration, angiogenesis, cell adhesion, cell polarity, spermatogenesis, and metastasis. Here, we show that JAM-C undergoes -palmitoylation on two juxtamembrane cysteine residues, Cys-264 and Cys-265. We have identified DHHC7 as a JAM-C palmitoylating enzyme by screening all known palmitoyltransferases (DHHCs). Ectopic expression of DHHC7, but not a DHHC7 catalytic mutant, enhances JAM-C -palmitoylation. Moreover, DHHC7 knockdown decreases the -palmitoylation level of JAM-C. Palmitoylation of JAM-C promotes its localization to tight junctions and inhibits transwell migration of A549 lung cancer cells. These results suggest that -palmitoylation of JAM-C can be potentially targeted to control cancer metastasis.
[Mh] Termos MeSH primário: Movimento Celular/fisiologia
Molécula C de Adesão Juncional/metabolismo
Lipoilação/fisiologia
Processamento de Proteína Pós-Traducional/fisiologia
Junções Íntimas/metabolismo
[Mh] Termos MeSH secundário: Células A549
Aciltransferases
Cisteína/metabolismo
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Peptídeos e Proteínas de Sinalização Intracelular/fisiologia
Células Jurkat
Ácido Palmítico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Intracellular Signaling Peptides and Proteins); 0 (Junctional Adhesion Molecule C); 0 (ZDHHC7 protein, human); 2V16EO95H1 (Palmitic Acid); EC 2.3.- (Acyltransferases); K848JZ4886 (Cysteine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170612
[Lr] Data última revisão:
170612
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170216
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.730523


  2 / 6 MEDLINE  
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[PMID]:27442505
[Au] Autor:Bradfield PF; Menon A; Miljkovic-Licina M; Lee BP; Fischer N; Fish RJ; Kwak B; Fisher EA; Imhof BA
[Ad] Endereço:Department of Pathology and Immunology, CMU, University of Geneva, 1211, rue Michel Servet 1, Geneva 4, Switzerland.
[Ti] Título:Divergent JAM-C Expression Accelerates Monocyte-Derived Cell Exit from Atherosclerotic Plaques.
[So] Source:PLoS One;11(7):e0159679, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Atherosclerosis, caused in part by monocytes in plaques, continues to be a disease that afflicts the modern world. Whilst significant steps have been made in treating this chronic inflammatory disease, questions remain on how to prevent monocyte and macrophage accumulation in atherosclerotic plaques. Junctional Adhesion Molecule C (JAM-C) expressed by vascular endothelium directs monocyte transendothelial migration in a unidirectional manner leading to increased inflammation. Here we show that interfering with JAM-C allows reverse-transendothelial migration of monocyte-derived cells, opening the way back out of the inflamed environment. To study the role of JAM-C in plaque regression we used a mouse model of atherosclerosis, and tested the impact of vascular JAM-C expression levels on monocyte reverse transendothelial migration using human cells. Studies in-vitro under inflammatory conditions revealed that overexpression or gene silencing of JAM-C in human endothelium exposed to flow resulted in higher rates of monocyte reverse-transendothelial migration, similar to antibody blockade. We then transplanted atherosclerotic, plaque-containing aortic arches from hyperlipidemic ApoE-/- mice into wild-type normolipidemic recipient mice. JAM-C blockade in the recipients induced greater emigration of monocyte-derived cells and further diminished the size of atherosclerotic plaques. Our findings have shown that JAM-C forms a one-way vascular barrier for leukocyte transendothelial migration only when present at homeostatic copy numbers. We have also shown that blocking JAM-C can reduce the number of atherogenic monocytes/macrophages in plaques by emigration, providing a novel therapeutic strategy for chronic inflammatory pathologies.
[Mh] Termos MeSH primário: Movimento Celular
Molécula C de Adesão Juncional/metabolismo
Monócitos/patologia
Placa Aterosclerótica/metabolismo
Placa Aterosclerótica/patologia
[Mh] Termos MeSH secundário: Animais
Anticorpos/farmacologia
Apolipoproteínas E/deficiência
Apolipoproteínas E/metabolismo
Artérias Carótidas/patologia
Movimento Celular/efeitos dos fármacos
Endotélio Vascular/efeitos dos fármacos
Endotélio Vascular/metabolismo
Endotélio Vascular/patologia
Citometria de Fluxo
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Inflamação/patologia
Junções Intercelulares/efeitos dos fármacos
Junções Intercelulares/metabolismo
Leucócitos/efeitos dos fármacos
Leucócitos/patologia
Lipídeos/sangue
Camundongos Endogâmicos C57BL
Modelos Biológicos
Monócitos/efeitos dos fármacos
Placa Aterosclerótica/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Apolipoproteins E); 0 (Junctional Adhesion Molecule C); 0 (Lipids)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160722
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0159679


  3 / 6 MEDLINE  
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[PMID]:27111582
[Au] Autor:Hintermann E; Bayer M; Ehser J; Aurrand-Lions M; Pfeilschifter JM; Imhof BA; Christen U
[Ad] Endereço:a Pharmazentrum Frankfurt/ZAFES, Goethe University Hospital Frankfurt , Frankfurt am Main , Germany.
[Ti] Título:Murine junctional adhesion molecules JAM-B and JAM-C mediate endothelial and stellate cell interactions during hepatic fibrosis.
[So] Source:Cell Adh Migr;10(4):419-33, 2016 Jul 03.
[Is] ISSN:1933-6926
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Classical junctional adhesion molecules JAM-A, JAM-B and JAM-C influence vascular permeability, cell polarity as well as leukocyte recruitment and immigration into inflamed tissue. As the vasculature becomes remodelled in chronically injured, fibrotic livers we aimed to determine distribution and role of junctional adhesion molecules during this pathological process. Therefore, livers of naïve or carbon tetrachloride-treated mice were analyzed by immunohistochemistry to localize all 3 classical junctional adhesion molecules. Hepatic stellate cells and endothelial cells were isolated and subjected to immunocytochemistry and flow cytometry to determine localization and functionality of JAM-B and JAM-C. Cells were further used to perform contractility and migration assays and to study endothelial tubulogenesis and pericytic coverage by hepatic stellate cells. We found that in healthy tissue, JAM-A was ubiquitously expressed whereas JAM-B and JAM-C were restricted to the vasculature. During fibrosis, JAM-B and JAM-C levels increased in endothelial cells and JAM-C was de novo generated in myofibroblastic hepatic stellate cells. Soluble JAM-C blocked contractility but increased motility in hepatic stellate cells. Furthermore, soluble JAM-C reduced endothelial tubulogenesis and endothelial cell/stellate cell interaction. Thus, during liver fibrogenesis, JAM-B and JAM-C expression increase on the vascular endothelium. More importantly, JAM-C appears on myofibroblastic hepatic stellate cells linking them as pericytes to JAM-B positive endothelial cells. This JAM-B/JAM-C mediated interaction between endothelial cells and stellate cells stabilizes vessel walls and may control the sinusoidal diameter. Increased hepatic stellate cell contraction mediated by JAM-C/JAM-C interaction may cause intrahepatic vasoconstriction, which is a major complication in liver cirrhosis.
[Mh] Termos MeSH primário: Comunicação Celular
Células Endoteliais/patologia
Células Estreladas do Fígado/patologia
Molécula B de Adesão Juncional/metabolismo
Molécula C de Adesão Juncional/metabolismo
Cirrose Hepática/metabolismo
Cirrose Hepática/patologia
[Mh] Termos MeSH secundário: Animais
Tetracloreto de Carbono
Comunicação Celular/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular
Movimento Celular/efeitos dos fármacos
Células Cultivadas
Colágeno/farmacologia
Combinação de Medicamentos
Células Endoteliais/efeitos dos fármacos
Células Endoteliais/metabolismo
Células Estreladas do Fígado/efeitos dos fármacos
Células Estreladas do Fígado/metabolismo
Junções Intercelulares/metabolismo
Laminina/farmacologia
Fígado/metabolismo
Fígado/patologia
Camundongos
Camundongos Endogâmicos C57BL
Miofibroblastos/efeitos dos fármacos
Miofibroblastos/metabolismo
Miofibroblastos/patologia
Ligação Proteica/efeitos dos fármacos
Proteoglicanas/farmacologia
Proteínas Recombinantes de Fusão/metabolismo
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drug Combinations); 0 (Junctional Adhesion Molecule B); 0 (Junctional Adhesion Molecule C); 0 (Laminin); 0 (Proteoglycans); 0 (Recombinant Fusion Proteins); 119978-18-6 (matrigel); 9007-34-5 (Collagen); CL2T97X0V0 (Carbon Tetrachloride)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160426
[St] Status:MEDLINE
[do] DOI:10.1080/19336918.2016.1178448


  4 / 6 MEDLINE  
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[PMID]:26311310
[Au] Autor:Economopoulou M; Avramovic N; Klotzsche-von Ameln A; Korovina I; Sprott D; Samus M; Gercken B; Troullinaki M; Grossklaus S; Funk RH; Li X; Imhof BA; Orlova VV; Chavakis T
[Ad] Endereço:Matina Economopoulou, Department of Ophthalmology, Univ. Hospital Carl Gustav Carus, TU Dresden, Fetscherstrasse 74, 01307, Dresden, Germany, Tel.: +49 351 45819291, E-mail: matina.economopoulou@uniklinikum-dresden.de.
[Ti] Título:Endothelial-specific deficiency of Junctional Adhesion Molecule-C promotes vessel normalisation in proliferative retinopathy.
[So] Source:Thromb Haemost;114(6):1241-9, 2015 Nov 25.
[Is] ISSN:0340-6245
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:In proliferative retinopathies, like proliferative diabetic retinopathy and retinopathy of prematurity (ROP), the hypoxia response is sustained by the failure of the retina to revascularise its ischaemic areas. Non-resolving retina ischaemia/hypoxia results in upregulation of pro-angiogenic factors and pathologic neovascularisation with ectopic, fragile neovessels. Promoting revascularisation of the retinal avascular area could interfere with this vicious cycle and lead to vessel normalisation. Here, we examined the function of endothelial junctional adhesion molecule-C (JAM-C) in the context of ROP. Endothelial-specific JAM-C-deficient (EC-JAM-C KO) mice and littermate JAM-C-proficient (EC-JAM-C WT) mice were subjected to the ROP model. An increase in total retinal vascularisation was found at p17 owing to endothelial JAM-C deficiency, which was the result of enhanced revascularisation and vessel normalisation, thereby leading to significantly reduced avascular area in EC-JAM-C KO mice. In contrast, pathologic neovessel formation was not affected by endothelial JAM-C deficiency. Consistent with improved vessel normalisation, tip cell formation at the interface between vascular and avascular area was higher in EC-JAM-C KO mice, as compared to their littermate controls. Consistently, JAM-C inactivation in endothelial cells resulted in increased spreading on fibronectin and enhanced sprouting in vitro in a manner dependent on ß1-integrin and on the activation of the small GTPase RAP1. Together, endothelial deletion of JAM-C promoted endothelial cell sprouting, and consequently vessel normalisation and revascularisation of the hypoxic retina without altering pathologic neovascularisation. Thus, targeting endothelial JAM-C may provide a novel therapeutic strategy for promoting revascularisation and vessel normalisation in the treatment of proliferative retinopathies.
[Mh] Termos MeSH primário: Endotélio Vascular/fisiopatologia
Molécula C de Adesão Juncional/deficiência
Neovascularização Patológica/fisiopatologia
Vasos Retinianos/fisiopatologia
Retinopatia da Prematuridade/fisiopatologia
Vitreorretinopatia Proliferativa/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Adesão Celular
Hipóxia Celular
Linhagem Celular
Tamanho Celular
Extensões da Superfície Celular
Modelos Animais de Doenças
Células Endoteliais
Endotélio Vascular/patologia
Fibronectinas
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Integrina beta1/fisiologia
Isquemia/fisiopatologia
Molécula C de Adesão Juncional/fisiologia
Camundongos
Camundongos Knockout
Neovascularização Patológica/etiologia
Especificidade de Órgãos
Molécula-1 de Adesão Celular Endotelial de Plaquetas/análise
Interferência de RNA
RNA Interferente Pequeno/genética
Vasos Retinianos/ultraestrutura
Proteínas rap1 de Ligação ao GTP/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fibronectins); 0 (Integrin beta1); 0 (Junctional Adhesion Molecule C); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (RNA, Small Interfering); EC 3.6.5.2 (rap1 GTP-Binding Proteins)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150828
[St] Status:MEDLINE
[do] DOI:10.1160/TH15-01-0051


  5 / 6 MEDLINE  
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[PMID]:23372751
[Au] Autor:Christen S; Coppieters K; Rose K; Holdener M; Bayer M; Pfeilschifter JM; Hintermann E; von Herrath MG; Aurrand-Lions M; Imhof BA; Christen U
[Ad] Endereço:Pharmazentrum Frankfurt/ZAFES, Goethe University Hospital, Frankfurt am Main, Germany. christen@med.uni-frankfurt.de
[Ti] Título:Blockade but not overexpression of the junctional adhesion molecule C influences virus-induced type 1 diabetes in mice.
[So] Source:PLoS One;8(1):e54675, 2013.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Type 1 diabetes (T1D) results from the autoimmune destruction of insulin-producing beta-cells in the pancreas. Recruitment of inflammatory cells is prerequisite to beta-cell-injury. The junctional adhesion molecule (JAM) family proteins JAM-B and JAM-C are involved in polarized leukocyte transendothelial migration and are expressed by vascular endothelial cells of peripheral tissue and high endothelial venules in lympoid organs. Blocking of JAM-C efficiently attenuated cerulean-induced pancreatitis, rheumatoid arthritis or inflammation induced by ischemia and reperfusion in mice. In order to investigate the influence of JAM-C on trafficking and transmigration of antigen-specific, autoaggressive T-cells, we used transgenic mice that express a protein of the lymphocytic choriomeningitis virus (LCMV) as a target autoantigen in the ß-cells of the islets of Langerhans under the rat insulin promoter (RIP). Such RIP-LCMV mice turn diabetic after infection with LCMV. We found that upon LCMV-infection JAM-C protein was upregulated around the islets in RIP-LCMV mice. JAM-C expression correlated with islet infiltration and functional beta-cell impairment. Blockade with a neutralizing anti-JAM-C antibody reduced the T1D incidence. However, JAM-C overexpression on endothelial cells did not accelerate diabetes in the RIP-LCMV model. In summary, our data suggest that JAM-C might be involved in the final steps of trafficking and transmigration of antigen-specific autoaggressive T-cells to the islets of Langerhans.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 1/imunologia
Diabetes Mellitus Tipo 1/virologia
Molécula C de Adesão Juncional/imunologia
Vírus da Coriomeningite Linfocítica/patogenicidade
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/imunologia
Anticorpos Neutralizantes/imunologia
Autoantígenos/genética
Autoantígenos/imunologia
Linhagem Celular
Diabetes Mellitus Tipo 1/genética
Células Endoteliais/metabolismo
Feminino
Expressão Gênica
Ilhotas Pancreáticas/imunologia
Ilhotas Pancreáticas/patologia
Ilhotas Pancreáticas/virologia
Molécula C de Adesão Juncional/antagonistas & inibidores
Molécula C de Adesão Juncional/genética
Vírus da Coriomeningite Linfocítica/imunologia
Masculino
Camundongos
Camundongos Transgênicos
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antibodies, Neutralizing); 0 (Autoantigens); 0 (Junctional Adhesion Molecule C)
[Em] Mês de entrada:1307
[Cu] Atualização por classe:150219
[Lr] Data última revisão:
150219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130202
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0054675


  6 / 6 MEDLINE  
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[PMID]:23029139
[Au] Autor:Wyss L; Schäfer J; Liebner S; Mittelbronn M; Deutsch U; Enzmann G; Adams RH; Aurrand-Lions M; Plate KH; Imhof BA; Engelhardt B
[Ad] Endereço:Theodor Kocher Institute, University of Bern, Bern, Switzerland.
[Ti] Título:Junctional adhesion molecule (JAM)-C deficient C57BL/6 mice develop a severe hydrocephalus.
[So] Source:PLoS One;7(9):e45619, 2012.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The junctional adhesion molecule (JAM)-C is a widely expressed adhesion molecule regulating cell adhesion, cell polarity and inflammation. JAM-C expression and function in the central nervous system (CNS) has been poorly characterized to date. Here we show that JAM-C(-/-) mice backcrossed onto the C57BL/6 genetic background developed a severe hydrocephalus. An in depth immunohistochemical study revealed specific immunostaining for JAM-C in vascular endothelial cells in the CNS parenchyma, the meninges and in the choroid plexus of healthy C57BL/6 mice. Additional JAM-C immunostaining was detected on ependymal cells lining the ventricles and on choroid plexus epithelial cells. Despite the presence of hemorrhages in the brains of JAM-C(-/-) mice, our study demonstrates that development of the hydrocephalus was not due to a vascular function of JAM-C as endothelial re-expression of JAM-C failed to rescue the hydrocephalus phenotype of JAM-C(-/-) C57BL/6 mice. Evaluation of cerebrospinal fluid (CSF) circulation within the ventricular system of JAM-C(-/-) mice excluded occlusion of the cerebral aqueduct as the cause of hydrocephalus development but showed the acquisition of a block or reduction of CSF drainage from the lateral to the 3(rd) ventricle in JAM-C(-/-) C57BL/6 mice. Taken together, our study suggests that JAM-C(-/-) C57BL/6 mice model the important role for JAM-C in brain development and CSF homeostasis as recently observed in humans with a loss-of-function mutation in JAM-C.
[Mh] Termos MeSH primário: Hidrocefalia/genética
Molécula C de Adesão Juncional/fisiologia
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Primers do DNA
Imunofluorescência
Molécula C de Adesão Juncional/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA Primers); 0 (Junctional Adhesion Molecule C)
[Em] Mês de entrada:1303
[Cu] Atualização por classe:150222
[Lr] Data última revisão:
150222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:121003
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0045619



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