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[PMID]:28931565
[Au] Autor:Ebnet K
[Ad] Endereço:Institute-Associated Research Group "Cell Adhesion and Cell Polarity", Institute of Medical Biochemistry, ZMBE, Cells-In-Motion Cluster of Excellence (EXC1003-CiM), and Interdisciplinary Clinical Research Center (IZKF), University of Münster, Münster, Germany.
[Ti] Título:Junctional Adhesion Molecules (JAMs): Cell Adhesion Receptors With Pleiotropic Functions in Cell Physiology and Development.
[So] Source:Physiol Rev;97(4):1529-1554, 2017 Oct 01.
[Is] ISSN:1522-1210
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Junctional adhesion molecules (JAM)-A, -B and -C are cell-cell adhesion molecules of the immunoglobulin superfamily which are expressed by a variety of tissues, both during development and in the adult organism. Through their extracellular domains, they interact with other adhesion receptors on opposing cells. Through their cytoplasmic domains, they interact with PDZ domain-containing scaffolding and signaling proteins. In combination, these two properties regulate the assembly of signaling complexes at specific sites of cell-cell adhesion. The multitude of molecular interactions has enabled JAMs to adopt distinct cellular functions such as the regulation of cell-cell contact formation, cell migration, or mitotic spindle orientation. Not surprisingly, JAMs regulate diverse processes such as epithelial and endothelial barrier formation, hemostasis, angiogenesis, hematopoiesis, germ cell development, and the development of the central and peripheral nervous system. This review summarizes the recent progress in the understanding of JAMs, including their characteristic structural features, their molecular interactions, their cellular functions, and their contribution to a multitude of processes during vertebrate development and homeostasis.
[Mh] Termos MeSH primário: Adesão Celular/fisiologia
Fenômenos Fisiológicos Celulares
Regulação da Expressão Gênica/fisiologia
Moléculas de Adesão Juncional/genética
Moléculas de Adesão Juncional/metabolismo
[Mh] Termos MeSH secundário: Animais
Imunoglobulinas/genética
Imunoglobulinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Immunoglobulins); 0 (Junctional Adhesion Molecules)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1152/physrev.00004.2017


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[PMID]:27522934
[Au] Autor:Marks FS; Almeida LL; Driemeier D; Canal C; Barcellos DE; Guimarães JA; Reck J
[Ad] Endereço:Centro Universitário UniRitter, Porto Alegre, RS, Brazil.
[Ti] Título:Porcine circovirus 2 (PCV2) increases the expression of endothelial adhesion/junction molecules.
[So] Source:Braz J Microbiol;47(4):870-875, 2016 Oct - Dec.
[Is] ISSN:1678-4405
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Porcine circovirus type 2 (PCV2) is the primary causative agent of porcine circovirus disease, a complex multisystem syndrome in domestic pigs. Despite the significant economic losses caused by porcine circovirus disease, the mechanisms of pathogenesis underlying the clinical findings remain largely unclear. As various reports have highlighted the potential key role of vascular lesions in the pathogenesis of porcine circovirus disease, the aim of this work was to investigate effects of PCV2 infection on vascular endothelial cells, focusing on cell viability and expression of adhesion/junction molecules. PCV2 infection reduced endothelial cell viability, while viral infection did not affected the viability of several other classical cell lines. Also, PCV2 infection in endothelial cells displayed a dual/biphasic effect: initially, infection increased ICAM-1 expression, which can favor leukocyte recruitment and emigration to tissues and possibly inducing characteristic porcine circovirus disease inflammatory lesions; then, secondarily, infection caused an increase in zonula occludens 1 tight junction protein (ZO-1) expression, which in turn can result in difficulties for cell traffic across the endothelium and a potential impairment the immune response in peripheral tissues. These virus-induced endothelial changes could directly impact the inflammatory process of porcine circovirus disease and associated vascular/immune system disturbances. Data suggest that, among the wide range of effects induced by PCV2 on the host, endothelial modulation can be a pivotal process which can help to explain PCV2 pathogenesis in some porcine circovirus disease presentations.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/genética
Infecções por Circoviridae/veterinária
Circovirus
Células Endoteliais/metabolismo
Expressão Gênica
Moléculas de Adesão Juncional/genética
Doenças dos Suínos/genética
Doenças dos Suínos/virologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Sobrevivência Celular
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (Junctional Adhesion Molecules)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160816
[St] Status:MEDLINE


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[PMID]:27515379
[Au] Autor:Reglero-Real N; Colom B; Bodkin JV; Nourshargh S
[Ad] Endereço:William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.
[Ti] Título:Endothelial Cell Junctional Adhesion Molecules: Role and Regulation of Expression in Inflammation.
[So] Source:Arterioscler Thromb Vasc Biol;36(10):2048-2057, 2016 Oct.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Endothelial cells line the lumen of all blood vessels and play a critical role in maintaining the barrier function of the vasculature. Sealing of the vessel wall between adjacent endothelial cells is facilitated by interactions involving junctionally expressed transmembrane proteins, including tight junctional molecules, such as members of the junctional adhesion molecule family, components of adherence junctions, such as VE-Cadherin, and other molecules, such as platelet endothelial cell adhesion molecule. Of importance, a growing body of evidence indicates that the expression of these molecules is regulated in a spatiotemporal manner during inflammation: responses that have significant implications for the barrier function of blood vessels against blood-borne macromolecules and transmigrating leukocytes. This review summarizes key aspects of our current understanding of the dynamics and mechanisms that regulate the expression of endothelial cells junctional molecules during inflammation and discusses the associated functional implications of such events in acute and chronic scenarios.
[Mh] Termos MeSH primário: Permeabilidade Capilar
Células Endoteliais/metabolismo
Inflamação/metabolismo
Junções Intercelulares/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Endoteliais/imunologia
Regulação da Expressão Gênica
Seres Humanos
Inflamação/genética
Inflamação/imunologia
Junções Intercelulares/imunologia
Moléculas de Adesão Juncional/genética
Moléculas de Adesão Juncional/imunologia
Moléculas de Adesão Juncional/metabolismo
Processamento de Proteína Pós-Traducional
Transporte Proteico
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Junctional Adhesion Molecules)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160813
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.116.307610


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[PMID]:27426071
[Au] Autor:Li YS; He WF; Wu J
[Ad] Endereço:Institute of Burn Research, Southwest Hospital, State Key Laboratory of Trauma, Burns and Combined Injury, the Third Military Medical University, Chongqing 400038, China.
[Ti] Título:[Advances in the research of biological characters and pathophysiological effects of dendritic epidermal T lymphocytes].
[So] Source:Zhonghua Shao Shang Za Zhi;32(1):58-61, 2016 Jan.
[Is] ISSN:1009-2587
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:The maturation of dendritic epidermal T lymphocytes (DETCs) in thymus needs ligand-mediated positive selection, and positive selection together with V3γ(+) γδT lymphocytes intrinsic program features order DETCs to specifically migrate to epidermis. Positive selection promotes DETCs to express CD122, which is vital for DETCs to survive and proliferate in skin. DETCs possess memory-like phenotype and are able to rapidly respond to danger signals when they move out from thymus. NKG2D, junctional adhesion molecule-like protein and 2B4 are demonstrated to participate in DETCs activation, except for ligands of T lymphocytes receptor. Effective DETCs secrete cytokines such as interferon-γ, insulin-like growth factor-2, keratinocyte growth factor and gain cytotoxicity to directly kill tumor cells. DETCs participate in skin immune surveillance, regulation of local inflammation, and wound healing promotion.
[Mh] Termos MeSH primário: Epiderme/citologia
Epiderme/imunologia
Linfócitos T/citologia
[Mh] Termos MeSH secundário: Antígenos CD/metabolismo
Movimento Celular
Fator 7 de Crescimento de Fibroblastos/metabolismo
Seres Humanos
Vigilância Imunológica
Inflamação/imunologia
Fator de Crescimento Insulin-Like II/metabolismo
Interferon gama/metabolismo
Subunidade beta de Receptor de Interleucina-2/metabolismo
Moléculas de Adesão Juncional/metabolismo
Subfamília K de Receptores Semelhantes a Lectina de Células NK
Receptores Imunológicos/metabolismo
Família de Moléculas de Sinalização da Ativação Linfocitária
Pele/imunologia
Timo/citologia
Cicatrização/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (CD244 protein, human); 0 (FGF7 protein, human); 0 (IFNG protein, human); 0 (IGF2 protein, human); 0 (Interleukin-2 Receptor beta Subunit); 0 (Junctional Adhesion Molecules); 0 (KLRK1 protein, human); 0 (NK Cell Lectin-Like Receptor Subfamily K); 0 (Receptors, Immunologic); 0 (Signaling Lymphocytic Activation Molecule Family); 126469-10-1 (Fibroblast Growth Factor 7); 67763-97-7 (Insulin-Like Growth Factor II); 82115-62-6 (Interferon-gamma)
[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:160719
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1009-2587.2016.01.018


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[PMID]:26865645
[Au] Autor:Wang B; Wu Z; Ji Y; Sun K; Dai Z; Wu G
[Ad] Endereço:State Key Laboratory of Animal Nutrition, China Agricultural University, Beijing, China; and.
[Ti] Título:L-Glutamine Enhances Tight Junction Integrity by Activating CaMK Kinase 2-AMP-Activated Protein Kinase Signaling in Intestinal Porcine Epithelial Cells.
[So] Source:J Nutr;146(3):501-8, 2016 Mar.
[Is] ISSN:1541-6100
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The tight junctions (TJs) are essential for maintenance of the intestinal mucosal barrier integrity. Results of our recent work show that dietary l-glutamine (Gln) supplementation enhances the protein abundance of TJ proteins in the small intestine of piglets. However, the underlying mechanisms remain largely unknown. OBJECTIVE: This study was conducted to test the hypothesis that Gln regulates TJ integrity through calcium/calmodulin-dependent kinase 2 (CaMKK2)-AMP-activated protein kinase (AMPK) signaling which, in turn, contributes to improved intestinal mucosal barrier function. METHODS: Jejunal enterocytes isolated from a newborn pig were cultured in the presence of 0-2.0 mmol Gln/L for indicated time points. Cell proliferation, monolayer transepithelial electrical resistance (TEER), paracellular permeability, expression and distribution of TJ proteins, and phosphorylated AMPK were determined. RESULTS: Compared with 0 mmol Gln/L, 2.0 mmol Gln/L enhanced (P < 0.05) cell growth (by 31.9% at 48 h and 11.1% at 60 h). Cells treated with 2 mmol Gln/L increased TEER by 32.2% at 60 h, and decreased (P < 0.05) TJ permeability by 20.3-40.0% at 36-60 h. In addition, 2.0 mmol Gln/L increased (P < 0.05) the abundance of transmembrane proteins, such as occludin, claudin-4, junction adhesion molecule (JAM)-A, and the plaque proteins zonula occludens (ZO)-1, ZO-2, and ZO-3 by 1.8-6 times. In contrast, 0.5 mmol Gln/L had a moderate effect on TJ protein abundance (20.2-70.5%; P < 0.05) of occludin, claudin-3, claudin-4, JAM-A, and ZO-1. 2.0 mmol Gln/L treatment led to a greater distribution of claudin-1, claudin-4, and ZO-1 at plasma membranes compared with 0 mmol Gln/L. This effect of Gln was mediated by the activation of CaMKK2-AMPK signaling, because either depletion of calcium from the medium or the presence of an inhibitor of CaMKK2 abrogated the effect of Gln on epithelial integrity. CONCLUSION: Our findings indicate that activation of CaMKK2-AMPK signaling by Gln is associated with improved intestinal mucosal barrier function through enhancing the abundance of TJ proteins and altering their intracellular localization in intestinal porcine epithelial cells.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Quinase da Proteína Quinase Dependente de Cálcio-Calmodulina/metabolismo
Células Epiteliais/efeitos dos fármacos
Glutamina/farmacologia
Transdução de Sinais
Junções Íntimas/efeitos dos fármacos
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/genética
Animais
Animais Recém-Nascidos
Quinase da Proteína Quinase Dependente de Cálcio-Calmodulina/genética
Membrana Celular/efeitos dos fármacos
Membrana Celular/metabolismo
Proliferação Celular/efeitos dos fármacos
Claudina-4/genética
Claudina-4/metabolismo
Enterócitos/citologia
Enterócitos/efeitos dos fármacos
Enterócitos/metabolismo
Células Epiteliais/metabolismo
Regulação da Expressão Gênica
Mucosa Intestinal/efeitos dos fármacos
Mucosa Intestinal/metabolismo
Intestinos/citologia
Intestinos/efeitos dos fármacos
Moléculas de Adesão Juncional/genética
Moléculas de Adesão Juncional/metabolismo
Ocludina/genética
Ocludina/metabolismo
Fosforilação
Suínos
Junções Íntimas/metabolismo
Proteína da Zônula de Oclusão-1/genética
Proteína da Zônula de Oclusão-1/metabolismo
Proteína da Zônula de Oclusão-2/genética
Proteína da Zônula de Oclusão-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Claudin-4); 0 (Junctional Adhesion Molecules); 0 (Occludin); 0 (Zonula Occludens-1 Protein); 0 (Zonula Occludens-2 Protein); 0RH81L854J (Glutamine); EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Kinase); EC 2.7.11.31 (AMP-Activated Protein Kinases)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160212
[St] Status:MEDLINE
[do] DOI:10.3945/jn.115.224857


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[PMID]:26595891
[Au] Autor:Murakami Y; Tanabe S; Suzuki T
[Ad] Endereço:Dept. of Biofunctional Science and Technology, Graduate School of Biosphere Science, Hiroshima Univ, Higashi-Hiroshima, Japan.
[Ti] Título:High-fat Diet-induced Intestinal Hyperpermeability is Associated with Increased Bile Acids in the Large Intestine of Mice.
[So] Source:J Food Sci;81(1):H216-22, 2016 Jan.
[Is] ISSN:1750-3841
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Metabolic syndrome is characterized by low-grade chronic systemic inflammation, which is associated with intestinal hyperpermeability. This study examined the effects of 3 high-fat diets (HFDs) composed of different fat sources (soybean oil and lard) on the intestinal permeability, tight junction (TJ) protein expression, and cecal bile acid (BA) concentrations in mice, and then analyzed their interrelations. C57/BL6 mice were fed the control diet, HFD (soybean oil), HFD (lard), and HFD (mix; containing equal concentrations of soybean oil and lard) for 8 wk. Glucose tolerance, intestinal permeability, TJ protein expression, and cecal BA concentration were evaluated. Feeding with the 3 HDFs similarly increased body weight, liver weight, and fat pad weight, and induced glucose intolerance and intestinal hyperpermeability. The expression of TJ proteins, zonula occludens-2 and junctional adhesion molecule-A, were lower in the colons of the 3 HFD groups than in the control group (P < 0.05), and these changes appeared to be related to intestinal hyperpermeability. Feeding with HFDs increased total secondary BA (SBA) and total BA concentrations along with increases in some individual BAs in the cecum. Significant positive correlations between intestinal permeability and the concentrations of most SBAs, such as deoxycholic acid and ω-muricholic acids, were detected (P < 0.05). These results suggest that the HFD-induced intestinal hyperpermeability is associated with increased BA secretion. The abundance of SBAs in the large intestine may be responsible for the hyperpermeability.
[Mh] Termos MeSH primário: Ácidos e Sais Biliares/metabolismo
Dieta Hiperlipídica/efeitos adversos
Gorduras na Dieta/efeitos adversos
Enteropatias/etiologia
Intestino Grosso/patologia
Síndrome Metabólica/patologia
Junções Íntimas/metabolismo
[Mh] Termos MeSH secundário: Tecido Adiposo/metabolismo
Animais
Ceco/metabolismo
Ácidos Cólicos/metabolismo
Colo/metabolismo
Ácido Desoxicólico/metabolismo
Gorduras na Dieta/administração & dosagem
Inflamação/metabolismo
Enteropatias/metabolismo
Intestino Grosso/metabolismo
Moléculas de Adesão Juncional/metabolismo
Fígado
Masculino
Camundongos Endogâmicos C57BL
Óleo de Soja
Ganho de Peso
Proteína da Zônula de Oclusão-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bile Acids and Salts); 0 (Cholic Acids); 0 (Dietary Fats); 0 (Junctional Adhesion Molecules); 0 (Zonula Occludens-2 Protein); 005990WHZZ (Deoxycholic Acid); 39016-49-4 (muricholic acid); 8001-22-7 (Soybean Oil); SI6O3IW77Z (lard)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151124
[St] Status:MEDLINE
[do] DOI:10.1111/1750-3841.13166


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[PMID]:26463937
[Au] Autor:Fujii M; Sherchan P; Soejima Y; Doycheva D; Zhao D; Zhang JH
[Ad] Endereço:Department of Physiology, Loma Linda University, Loma Linda, CA, USA.
[Ti] Título:Cannabinoid Receptor Type 2 Agonist Attenuates Acute Neurogenic Pulmonary Edema by Preventing Neutrophil Migration after Subarachnoid Hemorrhage in Rats.
[So] Source:Acta Neurochir Suppl;121:135-9, 2016.
[Is] ISSN:0065-1419
[Cp] País de publicação:Austria
[La] Idioma:eng
[Ab] Resumo:We evaluated whether JWH133, a selective cannabinoid type 2 receptor (CB2R) agonist, prevented neurogenic pulmonary edema (NPE) after subarachnoid hemorrhage (SAH) by attenuating inflammation. Adult male rats were assigned to six groups: sham-operated, SAH with vehicle, SAH with JWH133 (0.3, 1.0, or 3.0 mg/kg) treatment 1 h after surgery, and SAH with JWH133 (1.0 mg/kg) at 1 h with a selective CB2R antagonist, SR144528 (3.0 mg/kg). The perforation model of SAH was performed and pulmonary wet-to-dry weight ratio was evaluated 24 and 72 h after surgery. Western blot analyses and immunohistochemistry were evaluated 24 h after surgery. JWH133 (1.0 mg/kg) significantly and most strongly improved lung edema 24 h after SAH. SR144528 administration significantly reversed the effects of JWH133 (1.0 mg/kg). SAH-induced increasing levels of myeloperoxidase (MPO) and decreasing levels of a tight junction (TJ) protein, junctional adhesion molecule (JAM)-A, were ameliorated by JWH133 (1.0 mg/kg) administration 24 h after SAH. Immunohistochemical assessment also confirmed substantial leukocyte infiltration in the outside of vessels in SAH, which were attenuated by JWH133 (1.0 mg/kg) injection. CB2R agonist ameliorated lung permeability by inhibiting leukocyte trafficking and protecting tight junction proteins in the lung of NPE after SAH.
[Mh] Termos MeSH primário: Agonistas de Receptores de Canabinoides/farmacologia
Canabinoides/farmacologia
Movimento Celular/efeitos dos fármacos
Pulmão/efeitos dos fármacos
Neutrófilos/efeitos dos fármacos
Edema Pulmonar/patologia
Receptor CB2 de Canabinoide/agonistas
Hemorragia Subaracnóidea/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Bornanos/farmacologia
Antagonistas de Receptores de Canabinoides/farmacologia
Modelos Animais de Doenças
Imuno-Histoquímica
Moléculas de Adesão Juncional/metabolismo
Pulmão/metabolismo
Pulmão/patologia
Masculino
Tamanho do Órgão
Peroxidase/metabolismo
Edema Pulmonar/etiologia
Edema Pulmonar/metabolismo
Pirazóis/farmacologia
Ratos
Ratos Sprague-Dawley
Receptor CB2 de Canabinoide/antagonistas & inibidores
Hemorragia Subaracnóidea/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (1,1-dimethylbutyl-1-deoxy-Delta(9)-THC); 0 (Bornanes); 0 (Cannabinoid Receptor Agonists); 0 (Cannabinoid Receptor Antagonists); 0 (Cannabinoids); 0 (Junctional Adhesion Molecules); 0 (Pyrazoles); 0 (Receptor, Cannabinoid, CB2); 0 (SR 144528); EC 1.11.1.7 (Peroxidase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151015
[St] Status:MEDLINE
[do] DOI:10.1007/978-3-319-18497-5_24


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[PMID]:26434620
[Au] Autor:Liu C; Wang M; Jiang S; Wang L; Chen H; Liu Z; Qiu L; Song L
[Ad] Endereço:Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China; University of Chinese Academy of Sciences, Beijing 100049, China.
[Ti] Título:A novel junctional adhesion molecule A (CgJAM-A-L) from oyster (Crassostrea gigas) functions as pattern recognition receptor and opsonin.
[So] Source:Dev Comp Immunol;55:211-20, 2016 Feb.
[Is] ISSN:1879-0089
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Junctional adhesion molecule (JAM), a subfamily of immunoglobulin superfamily (IgSF) with a couple of immunoglobulin domains, can act as regulator in homeostasis and inflammation of vertebrates. In the present study, a structural homolog of JAM-A (designated CgJAM-A-L) was screened out from oyster, Crassostrea gigas, through a search of JAM-A D1 domain (N-terminal Ig domain in JAM-A). The cDNA of CgJAM-A-L was of 1188 bp encoding a predicted polypeptide of 395 amino acids. The immunoreactive area of CgJAM-A-L mainly distributed over the plasma membrane of hemocytes. After Vibro splendidus or tumor necrosis factor (CgTNF-1) stimulation, the mRNA transcripts of CgJAM-A-L in hemocytes increased significantly by 4.46-fold and 9.00-fold (p < 0.01) of those in control group, respectively. The recombinant CgJAM-A-L protein (rCgJAM-A-L) could bind multiple PAMPs including lipopolysaccharides (LPS), peptidoglycan (PGN), lipoteichoic acid (LTA), mannose (MAN), ß-glucan (GLU) and poly(I:C), and various microorganisms including Micrococcus luteus, Staphylococcus aureus, Escherichia coli, Vibro anguillarum, V. splendidus, Pastoris pastoris and Yarrowia lipolytica. The phagocytic rates of oyster hemocytes towards Gram-negative bacteria V. anguillarum and yeast P. pastoris were significantly enhanced after the incubation of rCgJAM-A-L, and even increased more significantly after the pre-incubation of rCgJAM-A-L with microbes (p < 0.01). The results collectively indicated that CgJAM-A-L functioned as an important pattern recognition receptor (PRR) and opsonin in the immune defense against invading pathogen in oyster. Moreover, as the most primitive specie with homolog of JAMs, the information of CgJAM-A-L in oyster would provide useful clues for the evolutionary study of JAMs and immunoglobulins.
[Mh] Termos MeSH primário: Infecções Bacterianas/imunologia
Hemócitos/fisiologia
Moléculas de Adesão Juncional/metabolismo
Micoses/imunologia
Proteínas Opsonizantes/metabolismo
Ostreidae/imunologia
Receptores de Reconhecimento de Padrão/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Células Cultivadas
Clonagem Molecular
Hemócitos/microbiologia
Imunidade Inata
Moléculas de Adesão Juncional/genética
Dados de Sequência Molecular
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Junctional Adhesion Molecules); 0 (Opsonin Proteins); 0 (Receptors, Pattern Recognition)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:151219
[Lr] Data última revisão:
151219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151006
[St] Status:MEDLINE


  9 / 152 MEDLINE  
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[PMID]:26424381
[Au] Autor:Sadowska GB; Ahmedli N; Chen X; Stonestreet BS
[Ad] Endereço:Department of Pediatrics, The Alpert Medical School of Brown University, Women & Infants Hospital of Rhode Island, Providence, RI 02905, United States.
[Ti] Título:Ontogeny of tight junction protein expression in the ovine cerebral cortex during development.
[So] Source:Neuroscience;310:422-9, 2015 Dec 03.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tight junctions of the blood-brain barrier are composed of transmembrane and associated cytoplasmic proteins. The transmembrane claudin proteins form the primary seal between endothelial cells and junctional adhesion molecules (JAMs) regulate tight junction formation. We have previously shown that claudin-1, claudin-5, zonula occludens (ZO)-1, and ZO-2 exhibit differential developmental regulation from 60% of gestation up to maturity in adult sheep. The purpose of the current study was to examine developmental changes in claudin-3, -12, and JAM-A protein expression in cerebral cortices of fetuses at 60%, 80%, and 90% gestation, and in newborn and adult sheep. We also examined correlations between changes in endogenous cortisol levels and tight junction protein expression in cerebral cortices of the fetuses. Claudin-3, -12 and JAM-A expressions were determined by Western immunoblot. Claudin-3 and -12 were lower (P<0.01) at 60%, 80%, 90% and in newborns than in adults, and JAM-A was lower in adults than in fetuses at 80% and 90% gestation. Claudin-3 expression demonstrated a direct correlation with increasing plasma cortisol levels (r=0.60, n=15, P<0.02) in the fetuses. We conclude that: claudin-3, -12 and JAM-A are expressed as early as 60% of gestation in ovine cerebral cortices, exhibit differential developmental regulation, and that increasing endogenous glucocorticoids modulate claudin-3 expression in the fetus.
[Mh] Termos MeSH primário: Córtex Cerebral/embriologia
Córtex Cerebral/metabolismo
Claudinas/metabolismo
Moléculas de Adesão Juncional/metabolismo
[Mh] Termos MeSH secundário: Animais
Claudina-3/metabolismo
Ovinos
Junções Íntimas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Claudin-3); 0 (Claudins); 0 (Junctional Adhesion Molecules)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151002
[St] Status:MEDLINE


  10 / 152 MEDLINE  
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[PMID]:26059553
[Au] Autor:Mahajan SD; Parikh NU; Woodruff TM; Jarvis JN; Lopez M; Hennon T; Cunningham P; Quigg RJ; Schwartz SA; Alexander JJ
[Ad] Endereço:Department of Medicine, University at Buffalo, Buffalo, NY, USA.
[Ti] Título:C5a alters blood-brain barrier integrity in a human in vitro model of systemic lupus erythematosus.
[So] Source:Immunology;146(1):130-43, 2015 Sep.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The blood-brain barrier (BBB) plays a crucial role in brain homeostasis, thereby maintaining the brain environment precise for optimal neuronal function. Its dysfunction is an intriguing complication of systemic lupus erythematosus (SLE). SLE is a systemic autoimmune disorder where neurological complications occur in 5-50% of cases and is associated with impaired BBB integrity. Complement activation occurs in SLE and is an important part of the clinical profile. Our earlier studies demonstrated that C5a generated by complement activation caused the loss of brain endothelial layer integrity in rodents. The goal of the current study was to determine the translational potential of these studies to a human system. To assess this, we used a two dimensional in vitro BBB model constructed using primary human brain microvascular endothelial cells and astroglial cells, which closely emulates the in vivo BBB allowing the assessment of BBB integrity. Increased permeability monitored by changes in transendothelial electrical resistance and cytoskeletal remodelling caused by actin fiber rearrangement were observed when the cells were exposed to lupus serum and C5a, similar to the observations in mice. In addition, our data show that C5a/C5aR1 signalling alters nuclear factor-κB translocation into nucleus and regulates the expression of the tight junction proteins, claudin-5 and zonula occludens 1 in this setting. Our results demonstrate for the first time that C5a regulates BBB integrity in a neuroinflammatory setting where it affects both endothelial and astroglial cells. In addition, we also demonstrate that our previous findings in a mouse model, were emulated in human cells in vitro, bringing the studies one step closer to understanding the translational potential of C5a/C5aR1 blockade as a promising therapeutic strategy in SLE and other neurodegenerative diseases.
[Mh] Termos MeSH primário: Barreira Hematoencefálica/metabolismo
Complemento C5a/metabolismo
Lúpus Eritematoso Sistêmico/patologia
Receptor da Anafilatoxina C5a/metabolismo
[Mh] Termos MeSH secundário: Citoesqueleto de Actina/metabolismo
Transporte Ativo do Núcleo Celular
Adolescente
Astrócitos/imunologia
Encéfalo/irrigação sanguínea
Células Cultivadas
Criança
Claudina-5/biossíntese
Ativação do Complemento/imunologia
Complemento C5a/imunologia
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
Impedância Elétrica
Células Endoteliais/imunologia
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Feminino
Seres Humanos
Moléculas de Adesão Juncional/biossíntese
Lúpus Eritematoso Sistêmico/imunologia
Masculino
NF-kappa B/metabolismo
Transporte Proteico
Receptor da Anafilatoxina C5a/antagonistas & inibidores
Receptor da Anafilatoxina C5a/imunologia
Junções Íntimas/metabolismo
Proteína da Zônula de Oclusão-1/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (C5AR1 protein, human); 0 (CLDN5 protein, human); 0 (CREB1 protein, human); 0 (Claudin-5); 0 (Cyclic AMP Response Element-Binding Protein); 0 (Junctional Adhesion Molecules); 0 (NF-kappa B); 0 (Receptor, Anaphylatoxin C5a); 0 (Zonula Occludens-1 Protein); 80295-54-1 (Complement C5a); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150611
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12489



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