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  • 1
    Online Resource
    Online Resource
    Experimental heart failure causes depression-like behavior together with differential regulation of inflammatory and structural genes in the brain
    Frontiers Media SA ; 2014
    In:  Frontiers in Behavioral Neuroscience Vol. 8 ( 2014-10-31)
    Details
    In: Frontiers in Behavioral Neuroscience, Frontiers Media SA, Vol. 8 ( 2014-10-31)
    Type of Medium: Online Resource
    ISSN: 1662-5153
    URL: Article
    DOI: 10.3389/fnbeh.2014.00376
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2014
    detail.hit.zdb_id: 2452960-6
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  • 2
    Online Resource
    Online Resource
    Toll-like receptors as potential therapeutic targets in cardiac dysfunction
    Informa UK Limited ; 2011
    In:  Expert Opinion on Therapeutic Targets Vol. 15, No. 6 ( 2011-06), p. 753-765
    Details
    In: Expert Opinion on Therapeutic Targets, Informa UK Limited, Vol. 15, No. 6 ( 2011-06), p. 753-765
    Type of Medium: Online Resource
    ISSN: 1472-8222 , 1744-7631
    URL: Article
    DOI: 10.1517/14728222.2011.566560
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2011
    detail.hit.zdb_id: 2028202-3
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  • 3
    Online Resource
    Online Resource
    5-Lipoxygenase facilitates healing after myocardial infarction
    Springer Science and Business Media LLC ; 2013
    In:  Basic Research in Cardiology Vol. 108, No. 4 ( 2013-7)
    Details
    In: Basic Research in Cardiology, Springer Science and Business Media LLC, Vol. 108, No. 4 ( 2013-7)
    Type of Medium: Online Resource
    ISSN: 0300-8428 , 1435-1803
    URL: Article
    DOI: 10.1007/s00395-013-0367-8
    RVK:
    XA 31125
    RVK:
    XA 10000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2013
    detail.hit.zdb_id: 1458470-0
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  • 4
    Online Resource
    Online Resource
    Conditional Overexpression of Neuronal Nitric Oxide Synthase Is Cardioprotective in Ischemia/Reperfusion
    Ovid Technologies (Wolters Kluwer Health) ; 2010
    In:  Circulation Vol. 122, No. 16 ( 2010-10-19), p. 1588-1603
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 122, No. 16 ( 2010-10-19), p. 1588-1603
    Abstract: We previously demonstrated that conditional overexpression of neuronal nitric oxide synthase (nNOS) inhibited L-type Ca 2+ channels and decreased myocardial contractility. However, nNOS has multiple targets within the cardiac myocyte. We now hypothesize that nNOS overexpression is cardioprotective after ischemia/reperfusion because of inhibition of mitochondrial function and a reduction in reactive oxygen species generation. Methods and Results— Ischemia/reperfusion injury in wild-type mice resulted in nNOS accumulation in the mitochondria. Similarly, transgenic nNOS overexpression caused nNOS abundance in mitochondria. nNOS translocation into the mitochondria was dependent on heat shock protein 90. Ischemia/reperfusion experiments in isolated hearts showed a cardioprotective effect of nNOS overexpression. Infarct size in vivo was also significantly reduced. nNOS overexpression also caused a significant increase in mitochondrial nitrite levels accompanied by a decrease of cytochrome c oxidase activity. Accordingly, O 2 consumption in isolated heart muscle strips was decreased in nNOS-overexpressing nNOS + /αMHC-tTA + mice already under resting conditions. Additionally, we found that the reactive oxygen species concentration was significantly decreased in hearts of nNOS-overexpressing nNOS + /αMHC-tTA + mice compared with noninduced nNOS + /αMHC-tTA + animals. Conclusion— We demonstrated that conditional transgenic overexpression of nNOS resulted in myocardial protection after ischemia/reperfusion injury. Besides a reduction in reactive oxygen species generation, this might be caused by nitrite-mediated inhibition of mitochondrial function, which reduced myocardial oxygen consumption already under baseline conditions.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.109.933630
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2010
    detail.hit.zdb_id: 1466401-X
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  • 5
    Online Resource
    Online Resource
    Abstract 211: Regulatory T cells improve healing after myocardial infarction
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Circulation Research Vol. 113, No. suppl_1 ( 2013-08)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 113, No. suppl_1 ( 2013-08)
    Abstract: Background: The proinflammatory activation of innate immunity by myocardial ischemic injury has been recognized for long time. Our recent data have indicated that activation of CD4+ T cells, presumably by auto-antigen recognition, is a prerequisite for formation of a stable scar and prevention from left ventricular dilation after experimental myocardial infarction in mice. We here hypothesized that regulatory CD4+CD25+Foxp3+CD4+ T cells might improve left ventricular wound healing and prevent from adverse remodeling after myocardial infarction. Results: Experimental myocardial infarction in mice induced the proliferation and activation of CD4+CD25+Foxp3+ regulatory T cells, as demonstrated by intracellular expression of the Ikaros family transcription factor Helios, in heart draining lymph nodes. Pretreatment of mice with an anti-CD25 antibody before myocardial infarction efficiently depleted CD4+CD25+Foxp3+ regulatory T cells and increased mortality after myocardial infarction as compared to mice treated with an isotype-matched control antibody of irrelevant specificity, i.e., 25% survival in anti-CD25 treated mice vs. 55,9% survival in control antibody treated animals. Therapeutic activation of regulatory CD4+CD25+Foxp3+ T cells by a superagonistic anti-CD28 antibody (CD28-SA) applied at day 2 after myocardial infarction prevented, compared to mice treated with an isotype-matched control antibody, from left ventricular rupture and resulted in improved survival (47.1% survival in the control group vs. 76.6% survival in the CD28-SA treated group). CD28-SA treatment lead to expansion of CD4+CD25+Foxp3+ T-cells in the peripheral blood and increased their frequency in the infarcted myocardium. This was associated with increased expression of several molecules known to facilitate wound healing by promoting the formation of a stable scar such as osteopontin and coagulation factor XIII. Conclusion: CD4+CD25+Foxp3+ regulatory T-cells are a prerequisite for proper myocardial wound healing and can be therapeutically activated to improve outcome after experimental myocardial infarction.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.113.suppl_1.A211
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
    detail.hit.zdb_id: 1467838-X
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  • 6
    Online Resource
    Online Resource
    Abstract 17530: Characterization of Cardiac-resident Leukocyte Populations in the Steady-state and During Aging
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Circulation Vol. 130, No. suppl_2 ( 2014-11-25)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 130, No. suppl_2 ( 2014-11-25)
    Abstract: Although it is well acknowledged that immunological phenomena participate in several cardiac diseases, it has been deeply neglected the fact that the heart is already populated by resident leukocytes before the onset of any sign of disease. In the present work we comprehensively characterized the cardiac-resident leukocyte populations and addressed for the first time in the literature how these cells take part in cardiac physiology and aging. We compared cardiac function, structure and gene expression of healthy naïve C57BL6/J (WT) mice 10 (young), 30 (mid-aged) and 60 (aged) wk old. Flow cytometrical analysis of perfused-digested murine hearts revealed a cardiac-resident leukocyte population comprised of approx. 103 cells/mg (M2-macrophages 〉 B-cells 〉 T-cells 〉 granulocytes). The frequency of resident leukocytes found in cardiac muscle was 17.4 fold higher than in skeletal muscle, suggesting that they might be relevant for cardiac physiology. Importantly, cardiac-resident leukocyte composition shifted towards a pro-inflammatory profile during aging. Additionally, qPCR analysis indicated a significant up-regulation of pro-inflammatory genes such as TNF, IL-1β and IFN-γ in aged mice (e.g. TNF mRNA expression level: 2.1 .10-4 ± 2.0 10-5 in young vs 1.5 .10-3 ± 2.6 .10-4 in aged mice; P 〈 0.05). Similar results were found regarding to pro-fibrotic and pro-hypertrophic genes expression (e.g. Coll-III, TGF-β and βMyHC). Furthermore, aged WT mice presented increased serum levels of autoantibodies against myosin and higher frequencies of activated T helper cells (CD4+CD69+) in mediastinal lymph nodes as compared to young mice. Echocardiographic and hemodynamic studies revealed that in parallel with increased inflammation, 60 wk old naïve mice spontaneously develop severe cardiac dysfunction (e.g. ejection fraction: 34.6% ± 5.19%). Altogether, these data demonstrated that the heart comprises an important and yet underappreciated resident leukocyte population in the steady-state and that shifts in its composition occur in parallel with the cardiac deterioration observed in aged mice.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.130.suppl_2.17530
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 1466401-X
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  • 7
    Online Resource
    Online Resource
    Abstract 212: Cd4+ T-cell Activation By T-cell Receptor Engagement Contributes To Myocardial Ischemia-reperfusion Injury
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Circulation Research Vol. 113, No. suppl_1 ( 2013-08)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 113, No. suppl_1 ( 2013-08)
    Abstract: Background: We have recently shown that CD4 + but not CD8 + T-cells contribute to ischemia-reperfusion injury of the myocardium. We therefore hypothesized that CD4 + T-cells become activated by autoantigen recognition via their T-cell receptor during reperfusion. Methods and Results: Infarct size as percent of the area-at-risk was determined by combined Evans` blue and triphenyltetrazolium (TTC) staining after 30 minutes of in vivo ischemia followed by 24 hours reperfusion in mice. After 24 hours of reperfusion there was a significantly increased population of CD4 + T-cells which expressed the surface protein CD40L in comparison to sham operated mice [n≥7; p 〈 0.05; WT 10.8 ± 0.2% vs. sham 6.4 ± 0.5%]. CD40L is typically expressed in T-cells activated by T-cell receptor engagement. OT-II mice carry a transgenic T-cell receptor with specificity for an ovalbumin-derived peptide. These mice have a limited T-cell receptor repertoire, dominated by specificity for the irrelevant antigen ovalbumin. After 30 minutes of ischemia and 24 hours of reperfusion OT-II mice showed significantly reduction in infarct size [n≥4; p= 0.02; infarct/area at risk: OTII mice 38.9 ± 2.4% vs. WT mice 63.7 ± 6.6 % ] . Administration of a CD40L blocking antibody to wildtype mice also reduced infarct size when compared to administration of isotype-matched antibodies [n≥6; p = 0.03; infarct/ area at risk: anti-CD154 treatment 60.4 ± 3.4% vs. control 75.3 ± 4.1%]. CD4 + CD25 + Foxp3 + T-cells (natural T-regulatory cells) have a low activation threshold and constitute a T-cell subset with reactivity against autoantigens. Depletion of these cells by diphtheria-toxin application in a mouse model expressing the diphtheria-toxin receptor under the Foxp3 promotor also resulted in a significant reduction of infarct size when compared to diphtheria-toxin treated wildtype mice [n≥4; p=0.03; infarct/ area at risk: T reg -depleted DEREG mice 51.9± 3% vs. WT littermates 72.3± 2%]. Conclusion: Our results indicate that CD4 + T-cells that have been activated by an MHC class II/ T-cell receptor dependent mechanism, presumably by autoantigen recognition, contribute to myocardial ischemia-reperfusion injury.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.113.suppl_1.A212
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
    detail.hit.zdb_id: 1467838-X
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  • 8
    Online Resource
    Online Resource
    How can we cure a heart “in flame”? A translational view on inflammation in heart failure
    Springer Science and Business Media LLC ; 2013
    In:  Basic Research in Cardiology Vol. 108, No. 4 ( 2013-7)
    Details
    In: Basic Research in Cardiology, Springer Science and Business Media LLC, Vol. 108, No. 4 ( 2013-7)
    Type of Medium: Online Resource
    ISSN: 0300-8428 , 1435-1803
    URL: Article
    DOI: 10.1007/s00395-013-0356-y
    RVK:
    XA 31125
    RVK:
    XA 10000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2013
    detail.hit.zdb_id: 1458470-0
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  • 9
    Online Resource
    Online Resource
    A Collagen α2(I) Mutation Impairs Healing after Experimental Myocardial Infarction
    Elsevier BV ; 2012
    In:  The American Journal of Pathology Vol. 180, No. 1 ( 2012-01), p. 113-122
    Details
    In: The American Journal of Pathology, Elsevier BV, Vol. 180, No. 1 ( 2012-01), p. 113-122
    Type of Medium: Online Resource
    ISSN: 0002-9440
    URL: Article
    DOI: 10.1016/j.ajpath.2011.09.033
    RVK:
    XA 10000
    RVK:
    XA 19800
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2012
    detail.hit.zdb_id: 1480207-7
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  • 10
    Online Resource
    Online Resource
    Foxp3 + CD4 + T Cells Improve Healing After Myocardial Infarction by Modulating Monocyte/Macrophage Differentiation
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Circulation Research Vol. 115, No. 1 ( 2014-06-20), p. 55-67
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 115, No. 1 ( 2014-06-20), p. 55-67
    Abstract: An exaggerated or persistent inflammatory activation after myocardial infarction (MI) leads to maladaptive healing and subsequent remodeling of the left ventricle. Foxp3 + CD4 + regulatory T cells (T reg cells) contribute to inflammation resolution. Therefore, T reg cells might influence cardiac healing post-MI. Objective : Our aim was to study the functional role of T reg cells in wound healing post-MI in a mouse model of permanent left coronary artery ligation. Methods and Results : Using a model of genetic T reg -cell ablation (Foxp3 DTR mice), we depleted the T reg -cell compartment before MI induction, resulting in aggravated cardiac inflammation and deteriorated clinical outcome. Mechanistically, T reg -cell depletion was associated with M1-like macrophage polarization, characterized by decreased expression of inflammation-resolving and healing-promoting factors. The phenotype of exacerbated cardiac inflammation and outcome in T reg -cell–ablated mice could be confirmed in a mouse model of anti-CD25 monoclonal antibody–mediated depletion. In contrast, therapeutic T reg -cell activation by superagonistic anti-CD28 monoclonal antibody administration 2 days after MI led to improved healing and survival. Compared with control animals, CD28-SA–treated mice showed increased collagen de novo expression within the scar, correlating with decreased rates of left ventricular ruptures. Therapeutic T reg -cell activation induced an M2-like macrophage differentiation within the healing myocardium, associated with myofibroblast activation and increased expression of monocyte/macrophage-derived proteins fostering wound healing. Conclusions : Our data indicate that T reg cells beneficially influence wound healing after MI by modulating monocyte/macrophage differentiation. Moreover, therapeutic activation of T reg cells constitutes a novel approach to improve healing post-MI.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.115.303895
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 1467838-X
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