LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 6 of total 6

Search options

  1. Article ; Online: Connexin channel-dependent signaling pathways in inflammation.

    Scheckenbach, K E Ludwig / Crespin, Sophie / Kwak, Brenda R / Chanson, Marc

    Journal of vascular research

    2011  Volume 48, Issue 2, Page(s) 91–103

    Abstract: Inflammation is a highly regulated process with common but also specific characteristics in each tissue affected. Recruitment of leukocytes from the blood to the injured tissue is an important early step in the inflammatory cascade. This review ... ...

    Abstract Inflammation is a highly regulated process with common but also specific characteristics in each tissue affected. Recruitment of leukocytes from the blood to the injured tissue is an important early step in the inflammatory cascade. This review highlights the role of connexins (Cxs) in the regulation of both acute and chronic inflammatory processes. Cxs form gap junction channels that provide a cytoplasmic continuity between adjacent cells allowing the intercellular exchange of ions and metabolites. Their structural halves form connexons or hemichannels. Each of them consists of 6 Cx proteins and hemichannels not taking part in gap junction formation but facilitating the release of small molecules such as ATP. Based on the differential distribution of various Cxs in different tissues such as the brain, lung capillaries and large blood vessels, our aim was to analyze the specific roles of Cxs in the inflammatory process in these tissues. Three typical sites of inflammation were chosen to shed light on similarities and differences in several types of responses: (1) atherosclerosis as a model for chronic inflammation, (2) the lung as an example of acute inflammation and (3) the 'immune-privileged' environment of the brain to highlight specific reactions of the vasculature to ischemic damage and inflammation at this site.
    MeSH term(s) Acute Disease ; Animals ; Astrocytes/metabolism ; Atherosclerosis/metabolism ; Brain/blood supply ; Brain/immunology ; Brain/metabolism ; Capillaries/physiopathology ; Chronic Disease ; Connexins/metabolism ; Gap Junctions/metabolism ; Glutamic Acid/metabolism ; Humans ; Inflammation/metabolism ; Leukocytes/physiology ; Lung/blood supply ; Lung/immunology ; Lung/metabolism ; Mice ; Signal Transduction
    Chemical Substances Connexins ; Glutamic Acid (3KX376GY7L)
    Language English
    Publishing date 2011
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1105259-4
    ISSN 1423-0135 ; 1018-1172
    ISSN (online) 1423-0135
    ISSN 1018-1172
    DOI 10.1159/000316942
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 513: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  2. Article ; Online: Connexin40 controls endothelial activation by dampening NFκB activation.

    Denis, Jean-Francois / Scheckenbach, K E Ludwig / Pfenniger, Anna / Meens, Merlijn J / Krams, Rob / Miquerol, Lucile / Taffet, Steven / Chanson, Marc / Delmar, Mario / Kwak, Brenda R

    Oncotarget

    2017  Volume 8, Issue 31, Page(s) 50972–50986

    Abstract: Connexins are proteins forming gap junction channels for intercellular communication. Connexin40 (Cx40) is highly expressed by endothelial cells (ECs) of healthy arteries but this expression is lost in ECs overlying atherosclerotic plaques. Low/ ... ...

    Abstract Connexins are proteins forming gap junction channels for intercellular communication. Connexin40 (Cx40) is highly expressed by endothelial cells (ECs) of healthy arteries but this expression is lost in ECs overlying atherosclerotic plaques. Low/oscillatory shear stress observed in bends and bifurcations of arteries is atherogenic partly through activation of the pro-inflammatory NFκB pathway in ECs. In this study, we investigated the relation between shear stress, Cx40 and NFκB. Shear stress-modifying casts were placed around carotid arteries of mice expressing eGFP under the Cx40 promoter (
    Language English
    Publishing date 2017-03-22
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.16438
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  3. Article: Connexin Channel-Dependent Signaling Pathways in Inflammation

    Scheckenbach, K.E. Ludwig / Crespin, Sophie / Kwak, Brenda R. / Chanson, Marc

    Journal of Vascular Research

    2010  Volume 48, Issue 2, Page(s) 91–103

    Abstract: Inflammation is a highly regulated process with common but also specific characteristics in each tissue affected. Recruitment of leukocytes from the blood to the injured tissue is an important early step in the inflammatory cascade. This review ... ...

    Institution Departments of Pediatrics Pathology and Immunology, and Internal Medicine-Cardiology, Geneva University Hospitals and University of Geneva, Geneva, Switzerland
    Abstract Inflammation is a highly regulated process with common but also specific characteristics in each tissue affected. Recruitment of leukocytes from the blood to the injured tissue is an important early step in the inflammatory cascade. This review highlights the role of connexins (Cxs) in the regulation of both acute and chronic inflammatory processes. Cxs form gap junction channels that provide a cytoplasmic continuity between adjacent cells allowing the intercellular exchange of ions and metabolites. Their structural halves form connexons or hemichannels. Each of them consists of 6 Cx proteins and hemichannels not taking part in gap junction formation but facilitating the release of small molecules such as ATP. Based on the differential distribution of various Cxs in different tissues such as the brain, lung capillaries and large blood vessels, our aim was to analyze the specific roles of Cxs in the inflammatory process in these tissues. Three typical sites of inflammation were chosen to shed light on similarities and differences in several types of responses: (1) atherosclerosis as a model for chronic inflammation, (2) the lung as an example of acute inflammation and (3) the ‘immune-privileged’ environment of the brain to highlight specific reactions of the vasculature to ischemic damage and inflammation at this site.
    Keywords Cerebral inflammation ; Connexin ; Gap junctions ; Acute lung injury ; Atherosclerosis
    Language English
    Publishing date 2010-10-07
    Publisher S. Karger AG
    Publishing place Basel, Switzerland
    Document type Article
    Note Vascular Update
    ZDB-ID 1105259-4
    ISSN 1423-0135 ; 1018-1172
    ISSN (online) 1423-0135
    ISSN 1018-1172
    DOI 10.1159/000316942
    Database Karger publisher's database

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 513: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  4. Article ; Online: Prostaglandin E₂regulation of cystic fibrosis transmembrane conductance regulator activity and airway surface liquid volume requires gap junctional communication.

    Scheckenbach, K E Ludwig / Losa, Davide / Dudez, Tecla / Bacchetta, Marc / O'Grady, Scott / Crespin, Sophie / Chanson, Marc

    American journal of respiratory cell and molecular biology

    2010  Volume 44, Issue 1, Page(s) 74–82

    Abstract: ... Both pathways involve the release of prostaglandin E₂ (PGE₂) and the stimulation of their basolateral receptors ...

    Abstract Stimulation of the cystic fibrosis transmembrane conductance regulator (CFTR) by protease-activated receptors (PARs) at the basolateral membranes and by adenosine receptors (ADO-Rs) at the apical membrane maintain airway surface liquid (ASL) volume, which is required to ensure hydrated and clearable mucus. Both pathways involve the release of prostaglandin E₂ (PGE₂) and the stimulation of their basolateral receptors (EP-Rs). We sought to determine whether gap junctions contribute to the coordination of these pathways for modulating CFTR activity and mucus hydration. We used RT-PCR and Western blotting to determine connexin (Cx), CD73, and EP-R expression in a Calu-3 airway epithelial cell line grown on Transwell (Corning Costar, Cambridge, MA) inserts. We used dye coupling to evaluate gap junctional intercellular communication (GJIC). We used Ussing chamber studies and X-Z confocal microscopy to monitor Cl(-) secretion and ASL volume regulation. We found that connexin 43 (Cx43)-mediated GJIC was increased either by endogenous ADO after the hydrolysis of purine nucleotides by CD73 or by the direct activation of ADO-Rs. Inhibition of phospholipase A2 and cyclooxygenase prevented ADO-dependent increases in GJIC, suggesting the involvement of PGE₂. PGE₂ was found to increase GJIC markedly by stimulating EP4-Rs. The modulation of ADO signaling also affected the PAR-dependent activation of CFTR. The reduction of GJIC by CD73 or Cx43 inhibition prevented PAR-evoked CFTR currents in Ussing chambers. The inhibition of GJIC resulted in a failure of PGE₂ to increase ASL volume in Calu-3 cells and in primary cultures of well-differentiated human airway epithelial cells. Thus, gap junctions coordinate a signaling network comprising CFTR, ADO-Rs, PARs, and EP-Rs, and are required for ASL volume homeostasis.
    MeSH term(s) 5'-Nucleotidase/metabolism ; Adenosine/metabolism ; Blotting, Western ; Cell Communication/drug effects ; Cell Line ; Cell Polarity ; Chlorides/metabolism ; Connexins/metabolism ; Cyclooxygenase Inhibitors/pharmacology ; Cystic Fibrosis Transmembrane Conductance Regulator/genetics ; Cystic Fibrosis Transmembrane Conductance Regulator/metabolism ; Dinoprostone/metabolism ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; GPI-Linked Proteins/metabolism ; Gap Junctions/drug effects ; Gap Junctions/metabolism ; Homeostasis ; Humans ; Membrane Potentials ; Microscopy, Confocal ; Mucociliary Clearance/drug effects ; Mucus/metabolism ; Phospholipase A2 Inhibitors ; Phospholipases A2/metabolism ; RNA Interference ; Receptors, Prostaglandin E/metabolism ; Receptors, Purinergic P1/metabolism ; Respiratory Mucosa/drug effects ; Respiratory Mucosa/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction/drug effects ; Surface Properties ; Time Factors
    Chemical Substances CFTR protein, human ; Chlorides ; Connexins ; Cyclooxygenase Inhibitors ; GPI-Linked Proteins ; Phospholipase A2 Inhibitors ; Receptors, Prostaglandin E ; Receptors, Purinergic P1 ; Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6) ; Phospholipases A2 (EC 3.1.1.4) ; 5'-Nucleotidase (EC 3.1.3.5) ; NT5E protein, human (EC 3.1.3.5) ; Adenosine (K72T3FS567) ; Dinoprostone (K7Q1JQR04M)
    Language English
    Publishing date 2010-02-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2009-0361OC
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 2851: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  5. Article ; Online: Connexin43 modulates neutrophil recruitment to the lung.

    Sarieddine, Maya Z Richani / Scheckenbach, K E Ludwig / Foglia, Bernard / Maass, Karen / Garcia, Irène / Kwak, Brenda R / Chanson, Marc

    Journal of cellular and molecular medicine

    2009  Volume 13, Issue 11-12, Page(s) 4560–4570

    Abstract: Transmigration of neutrophils through the microvascular endothelium is a cardinal event of acute inflammation. It has been suggested that gap junctions made of connexin43 (Cx43) may serve as a conducting pathway to spread inflammatory signals within the ... ...

    Abstract Transmigration of neutrophils through the microvascular endothelium is a cardinal event of acute inflammation. It has been suggested that gap junctions made of connexin43 (Cx43) may serve as a conducting pathway to spread inflammatory signals within the lung capillary network. To determine whether Cx43 contributes to neutrophil transmigration in vivo, the number of transmigrated neutrophils was monitored in lungs of Cx43 mouse models subjected to inflammation by intratracheal instillations of Pseudomonas aeruginosa lipopolysaccharide (LPS). Cx43 was detected in inflamed lungs independently of neutrophil recruitment, whereas Cx43 up-regulation was not detected in mice genetically protected from inflammation. Mice heterozygous for the Cx43 gene (gja1) showed a 56% (P < 0.01) reduction in airway neutrophil count. In contrast, increased (P < 0.05) neutrophil recruitment in response to LPS was observed in a mouse model expressing a mutant Cx43 with enhanced channel conductivity. In vitro adhesion assays showed that reduced conductivity of Cx43 channels with (43)Gap26, a Cx43 blocking peptide, decreased adhesion of neutrophils to endothelial cells. Finally, we found that instillation of (43)Gap26 in inflamed lungs reduced neutrophil transmigration by 65% (P < 0.05). These results indicate that inflammatory mediators up-regulate alveolar Cx43 to promote neutrophil recruitment to the airspace. Cx43 may therefore represent a pharmacological target in lung diseases characterized by excessive neutrophil recruitment to the airways.
    MeSH term(s) Animals ; Bronchoalveolar Lavage Fluid ; Cell Adhesion/drug effects ; Cell Communication/drug effects ; Cell Line ; Connexin 43/metabolism ; Cytokines/metabolism ; Humans ; Inflammation/immunology ; Inflammation/pathology ; Inflammation Mediators/metabolism ; Lipopolysaccharides/administration & dosage ; Lipopolysaccharides/pharmacology ; Lung/drug effects ; Lung/immunology ; Lung/pathology ; Lymphocyte Count ; Mice ; Neutrophil Infiltration/drug effects ; Neutrophil Infiltration/immunology ; Peptides/pharmacology ; Pulmonary Alveoli/drug effects ; Pulmonary Alveoli/metabolism ; Pulmonary Alveoli/pathology
    Chemical Substances Connexin 43 ; Cytokines ; Gap 26 peptide ; Inflammation Mediators ; Lipopolysaccharides ; Peptides
    Language English
    Publishing date 2009-01-23
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2074559-X
    ISSN 1582-4934 ; 1582-4934 ; 1582-1838
    ISSN (online) 1582-4934
    ISSN 1582-4934 ; 1582-1838
    DOI 10.1111/j.1582-4934.2008.00654.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 5752: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  6. Article ; Online: RAD51C--a new human cancer susceptibility gene for sporadic squamous cell carcinoma of the head and neck (HNSCC).

    Scheckenbach, Kathrin / Baldus, Stephan E / Balz, Vera / Freund, Marcel / Pakropa, Petra / Sproll, Christoph / Schäfer, Karl-Ludwig / Wagenmann, Martin / Schipper, Jörg / Hanenberg, Helmut

    Oral oncology

    2013  Volume 50, Issue 3, Page(s) 196–199

    Abstract: Introduction: Head and neck squamous cell carcinomas (HNSSCs) are one of the leading causes of cancer-associated death worldwide. Although certain behavioral risk factors are well recognized as tumor promoting, there is very little known about the ... ...

    Abstract Introduction: Head and neck squamous cell carcinomas (HNSSCs) are one of the leading causes of cancer-associated death worldwide. Although certain behavioral risk factors are well recognized as tumor promoting, there is very little known about the presence of predisposing germline mutations in HNSCC patients.
    Methods: In this study, we analyzed 121 individuals with HNSCCs collected at our institution for germline alterations in the newly identified cancer susceptibility gene RAD51C.
    Results: Sequencing of all exons and the adjacent introns revealed five distinct heterozygous sequence deviations in RAD51C in seven patients (5.8%). A female patient without any other risk factors carried a germline mutation that disrupted the canonical splice acceptor site of exon 5 (c.706-2A>G).
    Conclusions: As there are only a few publications in the literature identifying germline mutations in head and neck cancer patients, our results provide the first indication that paralogs of RAD51, recently described as mutated in breast and ovarian cancer patients, might also be candidates for genetic risk factors in sporadic squamous cell carcinomas of the head and neck.
    MeSH term(s) Carcinoma, Squamous Cell/genetics ; DNA Mutational Analysis ; DNA-Binding Proteins/genetics ; Exons ; Female ; Genetic Predisposition to Disease ; Germ-Line Mutation ; Head and Neck Neoplasms/genetics ; Humans ; Introns ; Male ; Risk Factors
    Chemical Substances DNA-Binding Proteins ; RAD51C protein, human
    Language English
    Publishing date 2013-12-06
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1120465-5
    ISSN 1879-0593 ; 0964-1955 ; 1368-8375
    ISSN (online) 1879-0593
    ISSN 0964-1955 ; 1368-8375
    DOI 10.1016/j.oraloncology.2013.11.007
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 4869: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.A 456: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

To top