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  1. Article ; Online: Cardiac (myo)fibroblasts modulate the migration of monocyte subsets

    Kathleen Pappritz / Konstantinos Savvatis / Annika Koschel / Kapka Miteva / Carsten Tschöpe / Sophie Van Linthout

    Scientific Reports, Vol 8, Iss 1, Pp 1-

    2018  Volume 11

    Abstract: Abstract Cardiac fibroblasts play an important role in the regulation of the extracellular matrix and are newly recognized as inflammatory supporter cells. Interferon (IFN)-γ is known to counteract transforming growth factor (TGF)-ß1-induced ... ...

    Abstract Abstract Cardiac fibroblasts play an important role in the regulation of the extracellular matrix and are newly recognized as inflammatory supporter cells. Interferon (IFN)-γ is known to counteract transforming growth factor (TGF)-ß1-induced myofibroblast differentiation. This study aims at investigating in vitro how IFN-γ affects TGF-ß1-induced monocyte attraction. Therefore, C4 fibroblasts and fibroblasts obtained by outgrowth culture from the left ventricle (LV) of male C57BL6/j mice were stimulated with TGF-β1, IFN-γ and TGF-β1 + IFN-γ. Confirming previous studies, IFN-γ decreased the TGF-ß1-induced myofibroblast differentiation, as obviated by lower collagen I, III, α-smooth muscle actin (α-SMA), lysyl oxidase (Lox)-1 and lysyl oxidase-like (LoxL)-2 levels in TGF-β1 + IFN-γ- versus TGF-ß1-stimulated cardiac fibroblasts. TGF-β1 + IFN-γ-stimulated C4 and cardiac fibroblasts displayed a higher CC-chemokine ligand (CCL) 2, CCL7 and chemokine C-X3-C motif ligand (Cx3CL1) release versus sole TGF-ß1-stimulated fibroblasts. Analysis of migrated monocyte subsets towards the different conditioned media further revealed that sole TGF-β1- and IFN-γ-conditioned media particularly attracted Ly6Clow and Ly6Chigh monocytes, respectively, as compared to control media. In line with theses findings, TGF-β1 + IFN-γ-conditioned media led to a lower Ly6Clow/Ly6Chigh monocyte migration ratio compared to sole TGF-ß1 treatment. These differences in monocyte migration reflect the complex interplay of pro-inflammatory cytokines and pro-fibrotic factors in cardiac remodelling and inflammation.
    Keywords Medicine ; R ; Science ; Q
    Subject code 500
    Language English
    Publishing date 2018-04-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Mesenchymal stromal cells inhibit NLRP3 inflammasome activation in a model of Coxsackievirus B3-induced inflammatory cardiomyopathy

    Kapka Miteva / Kathleen Pappritz / Marzena Sosnowski / Muhammad El-Shafeey / Irene Müller / Fengquan Dong / Konstantinos Savvatis / Jochen Ringe / Carsten Tschöpe / Sophie Van Linthout

    Scientific Reports, Vol 8, Iss 1, Pp 1-

    2018  Volume 16

    Abstract: Abstract Inflammation in myocarditis induces cardiac injury and triggers disease progression to heart failure. NLRP3 inflammasome activation is a newly identified amplifying step in the pathogenesis of myocarditis. We previously have demonstrated that ... ...

    Abstract Abstract Inflammation in myocarditis induces cardiac injury and triggers disease progression to heart failure. NLRP3 inflammasome activation is a newly identified amplifying step in the pathogenesis of myocarditis. We previously have demonstrated that mesenchymal stromal cells (MSC) are cardioprotective in Coxsackievirus B3 (CVB3)-induced myocarditis. In this study, MSC markedly inhibited left ventricular (LV) NOD2, NLRP3, ASC, caspase-1, IL-1β, and IL-18 mRNA expression in CVB3-infected mice. ASC protein expression, essential for NLRP3 inflammasome assembly, increased upon CVB3 infection and was abrogated in MSC-treated mice. Concomitantly, CVB3 infection in vitro induced NOD2 expression, NLRP3 inflammasome activation and IL-1β secretion in HL-1 cells, which was abolished after MSC supplementation. The inhibitory effect of MSC on NLRP3 inflammasome activity in HL-1 cells was partly mediated via secretion of the anti-oxidative protein stanniocalcin-1. Furthermore, MSC application in CVB3-infected mice reduced the percentage of NOD2-, ASC-, p10- and/or IL-1β-positive splenic macrophages, natural killer cells, and dendritic cells. The suppressive effect of MSC on inflammasome activation was associated with normalized expression of prominent regulators of myocardial contractility and fibrosis to levels comparable to control mice. In conclusion, MSC treatment in myocarditis could be a promising strategy limiting the adverse consequences of cardiac and systemic NLRP3 inflammasome activation.
    Keywords Medicine ; R ; Science ; Q
    Subject code 570
    Language English
    Publishing date 2018-02-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Cardiac Fibroblasts Aggravate Viral Myocarditis

    Diana Lindner / Jia Li / Konstantinos Savvatis / Karin Klingel / Stefan Blankenberg / Carsten Tschöpe / Dirk Westermann

    Mediators of Inflammation, Vol

    Cell Specific Coxsackievirus B3 Replication

    2014  Volume 2014

    Keywords Pathology ; RB1-214 ; Medicine ; R
    Language English
    Publishing date 2014-01-01T00:00:00Z
    Publisher Hindawi Publishing Corporation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Cardiac Fibroblasts Aggravate Viral Myocarditis

    Diana Lindner / Jia Li / Konstantinos Savvatis / Karin Klingel / Stefan Blankenberg / Carsten Tschöpe / Dirk Westermann

    Mediators of Inflammation, Vol

    Cell Specific Coxsackievirus B3 Replication

    2014  Volume 2014

    Keywords Pathology ; RB1-214 ; Medicine ; R
    Language English
    Publishing date 2014-01-01T00:00:00Z
    Publisher Hindawi Publishing Corporation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Cardiac Fibroblasts Aggravate Viral Myocarditis

    Diana Lindner / Jia Li / Konstantinos Savvatis / Karin Klingel / Stefan Blankenberg / Carsten Tschöpe / Dirk Westermann

    Mediators of Inflammation, Vol

    Cell Specific Coxsackievirus B3 Replication

    2014  Volume 2014

    Keywords Pathology ; RB1-214 ; Medicine ; R
    Language English
    Publishing date 2014-01-01T00:00:00Z
    Publisher Hindawi Publishing Corporation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: CX3CR1 knockout aggravates Coxsackievirus B3-induced myocarditis.

    Irene Müller / Kathleen Pappritz / Konstantinos Savvatis / Kerstin Puhl / Fengquan Dong / Muhammad El-Shafeey / Nazha Hamdani / Isabell Hamann / Michel Noutsias / Carmen Infante-Duarte / Wolfgang A Linke / Sophie Van Linthout / Carsten Tschöpe

    PLoS ONE, Vol 12, Iss 8, p e

    2017  Volume 0182643

    Abstract: Studies on inflammatory disorders elucidated the pivotal role of the CX3CL1/CX3CR1 axis with respect to the pathophysiology and diseases progression. Coxsackievirus B3 (CVB3)-induced myocarditis is associated with severe cardiac inflammation, which may ... ...

    Abstract Studies on inflammatory disorders elucidated the pivotal role of the CX3CL1/CX3CR1 axis with respect to the pathophysiology and diseases progression. Coxsackievirus B3 (CVB3)-induced myocarditis is associated with severe cardiac inflammation, which may progress to heart failure. We therefore investigated the influence of CX3CR1 ablation in the model of acute myocarditis, which was induced by inoculation with 5x105 plaque forming units of CVB3 (Nancy strain) in either CX3CR1-/- or C57BL6/j (WT) mice. Seven days after infection, myocardial inflammation, remodeling, and titin expression and phosphorylation were examined by immunohistochemistry, real-time PCR and Pro-Q diamond stain. Cardiac function was assessed by tip catheter. Compared to WT CVB3 mice, CX3CR1-/- CVB3 mice exhibited enhanced left ventricular expression of inflammatory cytokines and chemokines, which was associated with an increase of immune cell infiltration/presence. This shift towards a pro-inflammatory immune response further resulted in increased cardiac fibrosis and cardiomyocyte apoptosis, which was reflected by an impaired cardiac function in CX3CR1-/- CVB3 compared to WT CVB3 mice. These findings demonstrate a cardioprotective role of CX3CR1 in CVB3-infected mice and indicate the relevance of the CX3CL1/CX3CR1 system in CVB3-induced myocarditis.
    Keywords Medicine ; R ; Science ; Q
    Subject code 616
    Language English
    Publishing date 2017-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: High-Mobility Group Box-1 Protein Serum Levels Do Not Reflect Monocytic Function in Patients with Sepsis-Induced Immunosuppression

    Petra Reinke / Joerg C. Schefold / Hans-Dieter Volk / Christina Fotopoulou / Ben Hammoud / Nadine Unterwalder / Konstantinos Savvatis / Christian Meisel

    Mediators of Inflammation, Vol

    2010  Volume 2010

    Keywords Pathology ; RB1-214 ; Medicine ; R ; DOAJ:Pathology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Language English
    Publishing date 2010-01-01T00:00:00Z
    Publisher Hindawi Publishing Corporation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Mesenchymal stromal cells but not cardiac fibroblasts exert beneficial systemic immunomodulatory effects in experimental myocarditis.

    Konstantinos Savvatis / Sophie van Linthout / Kapka Miteva / Kathleen Pappritz / Dirk Westermann / Joerg C Schefold / Gerhard Fusch / Alice Weithäuser / Ursula Rauch / Peter-Moritz Becher / Karin Klingel / Jochen Ringe / Andreas Kurtz / Heinz-Peter Schultheiss / Carsten Tschöpe

    PLoS ONE, Vol 7, Iss 7, p e

    2012  Volume 41047

    Abstract: Systemic application of mesenchymal stromal cells (MSCs) in inflammatory cardiomyopathy exerts cardiobeneficial effects. The mode of action is unclear since a sufficient and long-acting cardiac homing of MSCs is unlikely. We therefore investigated the ... ...

    Abstract Systemic application of mesenchymal stromal cells (MSCs) in inflammatory cardiomyopathy exerts cardiobeneficial effects. The mode of action is unclear since a sufficient and long-acting cardiac homing of MSCs is unlikely. We therefore investigated the regulation of the immune response in coxsackievirus B3 (CVB3)-induced acute myocarditis after intravenous application of MSCs. Wildtype mice were infected with CVB3 and treated with either PBS, human MSCs or human cardiac fibroblasts intravenously 1 day after infection. Seven days after infection, MSCs could be detected in the spleen, heart, pancreas, liver, lung and kidney, whereby the highest presence was observed in the lung. MSCs increased significantly the myocardial expression of HGF and decreased the expression of the proinflammatory cytokines TNFα, IL1β and IL6 as well as the severity of myocarditis and ameliorated the left ventricular dysfunction measured by conductance catheter. MSCs upregulated the production of IFNγ in CD4+ and CD8+ cells, the number of IL10-producing regulatory T cells and the apoptosis rate of T cells in the spleen. An increased number of CD4+CD25+FoxP3 could be found in the spleen as well as in the circulation. In contrast, application of human cardiac fibroblasts had no effect on the severity of myocarditis and the systemic immune response observed after MSCs-administration. In conclusion, modulation of the immune response in extracardiac organs is associated with cardiobeneficial effects in experimental inflammatory cardiomyopathy after systemic application of MSCs.
    Keywords Medicine ; R ; Science ; Q
    Subject code 570
    Language English
    Publishing date 2012-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Targeting LOXL2 for cardiac interstitial fibrosis and heart failure treatment

    Jin Yang / Konstantinos Savvatis / Jong Seok Kang / Peidong Fan / Hongyan Zhong / Karen Schwartz / Vivian Barry / Amanda Mikels-Vigdal / Serge Karpinski / Dmytro Kornyeyev / Joanne Adamkewicz / Xuhui Feng / Qiong Zhou / Ching Shang / Praveen Kumar / Dillon Phan / Mario Kasner / Begoña López / Javier Diez /
    Keith C. Wright / Roxanne L. Kovacs / Peng-Sheng Chen / Thomas Quertermous / Victoria Smith / Lina Yao / Carsten Tschöpe / Ching-Pin Chang

    Nature Communications, Vol 7, Iss 1, Pp 1-

    2016  Volume 15

    Abstract: Lysyl oxidase-like 2 (LOXL2) is an enzyme that promotes scaffolding of extracellular matrix proteins. Here the authors show that LOXL2 is crucial for pressure-overload induced cardiac fibrosis, and that antibody-mediated inhibition or genetic disruption ... ...

    Abstract Lysyl oxidase-like 2 (LOXL2) is an enzyme that promotes scaffolding of extracellular matrix proteins. Here the authors show that LOXL2 is crucial for pressure-overload induced cardiac fibrosis, and that antibody-mediated inhibition or genetic disruption ofLoxl2in mice shows therapeutic potential for treatment of cardiac fibrosis.
    Keywords Science ; Q
    Language English
    Publishing date 2016-12-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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