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38 results on '"Schuett, Harald"'

1. Sex-Specific Disparities in Outcomes of Transcatheter Edge-to-Edge Repair for Mitral Regurgitation: A Multicenter “Real-World” Analysis

Author

Ausbuettel, Felix, primary, Barth, Sebastian, additional, Chatzis, Georgios, additional, Sassani, Kiarash, additional, Fischer, Dieter, additional, Weyand, Sebastian, additional, Mueller, Julian, additional, Schuett, Harald, additional, Schieffer, Bernhard, additional, Luesebrink, Ulrich, additional, and Waechter, Christian, additional

Published
2023
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6. Case Report: Arterial Wall Inflammation in Atherosclerotic Cardiovascular Disease is Reduced by Olamkicept (sgp130Fc)

Author

Schulte, Dominik M., primary, Waetzig, Georg H., additional, Schuett, Harald, additional, Marx, Marlies, additional, Schulte, Berenice, additional, Garbers, Christoph, additional, Lokau, Juliane, additional, Vlacil, Ann-Kathrin, additional, Schulz, Juliane, additional, Seoudy, Anna K., additional, Schieffer, Bernhard, additional, Rosenstiel, Philip, additional, Seeger, Marcus, additional, Laudes, Matthias, additional, Rose-John, Stefan, additional, Lützen, Ulf, additional, Grote, Karsten, additional, and Schreiber, Stefan, additional

Published
2022
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8. Comparison of Mechanical Support with Impella or Extracorporeal Life Support in Post-Cardiac Arrest Cardiogenic Shock: A Propensity Scoring Matching Analysis

Author

Syntila, Styliani, primary, Chatzis, Georgios, additional, Markus, Birgit, additional, Ahrens, Holger, additional, Waechter, Christian, additional, Luesebrink, Ulrich, additional, Divchev, Dimitar, additional, Schuett, Harald, additional, Tsalouchidou, Panagiota-Eleni, additional, Jerrentrup, Andreas, additional, Parahuleva, Mariana, additional, Schieffer, Bernhard, additional, and Karatolios, Konstantinos, additional

Published
2021
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9. Left Ventricle Architecture and Valvular Integrity Following Microaxial Mechanical Support: A Two-Year Follow-Up Study

Author

Chatzis, Georgios, primary, Syntila, Styliani, additional, Schuett, Harald, additional, Waechter, Christian, additional, Ahrens, Holger, additional, Markus, Birgit, additional, Divchev, Dimitar, additional, Rogmann, Marc, additional, Karatolios, Konstantinos, additional, Bouras, Georgios, additional, Schieffer, Bernhard, additional, and Luesebrink, Ulrich, additional

Published
2021
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13. Identification of microRNAs involved in NOD-dependent induction of pro-inflammatory genes in pulmonary endothelial cells

Author

Vlacil, Ann-Kathrin, primary, Vollmeister, Evelyn, additional, Bertrams, Wilhelm, additional, Schoesser, Florian, additional, Oberoi, Raghav, additional, Schuett, Jutta, additional, Schuett, Harald, additional, Huehn, Sonja, additional, Bedenbender, Katrin, additional, Schmeck, Bernd T., additional, Schieffer, Bernhard, additional, and Grote, Karsten, additional

Published
2020
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16. Suppressor of Cytokine Signaling 1 is Involved in Gene Regulation Which Controls the Survival of Ly6Clow Monocytes in Mice.

Author

Schuett, Jutta, Kreutz, Julian, Grote, Karsten, Vlacil, Ann-Kathrin, Schuett, Harald, Oberoi, Raghav, Schmid, Andreas, Witten, Anika, Stoll, Monika, Schieffer, Bernhard, and Rühle, Frank

Subjects
CYTOKINES, MONOCYTES, MESSENGER RNA, PRINCIPAL components analysis, CHEMOKINE receptors
Abstract

Background/Aims: Inflammatory processes are controlled by the fine-tuned balance of monocyte subsets. In mice, different subsets of monocytes can be distinguished by the expression of Ly6C that is highly expressed on inflammatory monocytes (Ly6Chigh) and to a lesser extent on patrolling monocytes (Ly6Clow). Our previous study revealed an accumulation of Ly6Chigh monocytes in atherosclerotic-prone mice bearing a deficiency in suppressor of cytokine signaling (SOCS)-1 leading to an increased atherosclerotic burden. To decipher the underlying mechanisms, we performed a genome-wide analysis of SOCS-1-dependent gene regulation in Ly6Chigh and Ly6Clow monocytes. Methods: In monocyte subsets from SOCS-1- competent and -deficient mice differentially regulated genes were identified using an Illumina mRNA microarray (45,200 transcripts), which were randomly validated by qPCR. Principal component analysis was performed to further characterize mRNA profiles in monocyte subsets. To unravel potential regulatory mechanisms behind the differential mRNA expression, in silico analysis of a transcription factor (TF) network correlating with SOCS-1-dependent mRNA expression was carried out and combined with a weighted correlation network analysis (WGCNA). Results: mRNA analysis in monocyte subsets revealed 46 differentially regulated genes by 2-fold or more. Principal component analysis illustrated a distinct separation of mRNA profiles in monocyte subsets from SOCS-1-deficient mice. Notably, two cell surface receptors crucially involved in the determination of monocyte differentiation and survival, C-X3-C chemokine receptor 1 (CX3CR1) and colony stimulating factor 1 receptor (CSF1R), were identified to be regulated by SOCS-1. Moreover, in silico analysis of a TF network in combination with the WGCNA revealed genes coding for PPAR-γ, NUR77 and several ETSdomain proteins that act as pivotal inflammatory regulators. Conclusion: Our study reveals that SOCS-1 is implicated in a TF network regulating the expression of central transcription factors like PPAR-γ and NUR77 thereby influencing the expression of CX3CR1 and CSF1R that are known to be pivotal for the survival of Ly6Clow monocytes. [ABSTRACT FROM AUTHOR]

Published
2019
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21. Acute perioperative stress-induced increase of plaque volume and vulnerability in apolipoprotein E-deficient mice is amenable to statin treatment and IL-6-inhibition

Author

Janssen, Henrike, primary, Wagner, Christian S., additional, Demmer, Philipp, additional, Callies, Simone, additional, Sölter, Gesine, additional, Kouzhani, Houra Loghmani, additional, Hu, Niandan, additional, Schuett, Harald, additional, Tietge, Uwe J.F., additional, Warnecke, Gregor, additional, Larmann, Jan, additional, and Theilmeier, Gregor, additional

Published
2015
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22. NADPH oxidase NOX2 mediates TLR2/6-dependent release of GM-CSF from endothelial cells.

Author

Schuett, Jutta, Schuett, Harald, Oberoi, Raghav, Koch, Ann-Kathrin, Pretzer, Silke, Luchtefeld, Maren, Schieffer, Bernhard, and Grote, Karsten

Abstract

NADPH oxidase-generated reactive oxygen species (ROS) from immune cells are well known to be important for pathogen killing in response to TLR ligands. Here, we investigated a new aspect of NADPH oxidase in the TLR2/6-induced release of the immunologically relevant GM-CSF by endothelial cells. Stimulation of human endothelial cells with TLR2/6 agonist, MALP-2 (macrophage-activating lipopeptide of 2 kDa), induced NADPH oxidase activation and ROS formation. Inhibition by ROS scavengers and NADPH oxidase inhibitors blocked MALP-2-induced GM-CSF release. NADPH oxidase activators or ROS donors alone did not result in GM-CSF secretion; however, additional superoxide supply augmented MALP-2-induced GM-CSF secretion and restored GM-CSF levels after NADPH oxidase inhibition. MALP-2-dependent NF-ĸB activation was suppressed by NADPH oxidase inhibition, and inhibition of NF-κB completely blunted MALP-2-induced GM-CSF release. Vascular explants from mice that were deficient for the NADPH oxidase subunit p47phox showed diminished intimal superoxide production and GM-CSF release after ex vivo stimulation with MALP-2. Moreover, an increase in circulating progenitor cells after MALP-2 injection was completely abolished in p47phox-knockout mice. Finally, MALP-2 stimulation increased mRNA expression of the major subunit NADPH oxidase, (Nox)2, in endothelial cells, and Nox2 inhibition prevented MALP-2-induced GM-CSF release. Our findings identify a Nox2-containing NADPH oxidase as a crucial regulator of the immunologic important growth factor GM-CSF after TLR2/6 stimulation in endothelial cells. [ABSTRACT FROM AUTHOR]

Published
2017
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24. Toll-Like Receptor 2/6 Agonist Macrophage-Activating Lipopeptide-2 Promotes Reendothelialization and Inhibits Neointima Formation After Vascular Injury

Author

Grote, Karsten, primary, Sonnenschein, Kristina, additional, Kapopara, Piyushkumar R., additional, Hillmer, Anja, additional, Grothusen, Christina, additional, Salguero, Gustavo, additional, Kotlarz, Daniel, additional, Schuett, Harald, additional, Bavendiek, Udo, additional, and Schieffer, Bernhard, additional

Published
2013
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25. Experimental Gingivitis Induces Systemic Inflammatory Markers in Young Healthy Individuals: A Single-Subject Interventional Study

Author

Eberhard, Jörg, primary, Grote, Karsten, additional, Luchtefeld, Maren, additional, Heuer, Wieland, additional, Schuett, Harald, additional, Divchev, Dimitar, additional, Scherer, Ralph, additional, Schmitz-Streit, Ruth, additional, Langfeldt, Daniela, additional, Stumpp, Nico, additional, Staufenbiel, Ingmar, additional, Schieffer, Bernhard, additional, and Stiesch, Meike, additional

Published
2013
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26. Role of Suppressor of Cytokine Signaling-1 In Murine Atherosclerosis

Author

Grothusen, Christina, primary, Schuett, Harald, additional, Hillmer, Anja, additional, Lumpe, Stefan, additional, Grote, Karsten, additional, Ballmaier, Matthias, additional, Bleich, Andre, additional, Glage, Silke, additional, Tietge, Uwe J. F., additional, Luchtefeld, Maren, additional, and Schieffer, Bernhard, additional

Published
2012
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27. Transsignaling of Interleukin-6 Crucially Contributes to Atherosclerosis in Mice

Author

Schuett, Harald, primary, Oestreich, René, additional, Waetzig, Georg H., additional, Annema, Wijtske, additional, Luchtefeld, Maren, additional, Hillmer, Anja, additional, Bavendiek, Udo, additional, von Felden, Johann, additional, Divchev, Dimitar, additional, Kempf, Tibor, additional, Wollert, Kai C., additional, Seegert, Dirk, additional, Rose-John, Stefan, additional, Tietge, Uwe J.F., additional, Schieffer, Bernhard, additional, and Grote, Karsten, additional

Published
2012
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28. Chemokine Receptor 7 Knockout Attenuates Atherosclerotic Plaque Development

Author

Luchtefeld, Maren, primary, Grothusen, Christina, additional, Gagalick, Andreas, additional, Jagavelu, Kumaravelu, additional, Schuett, Harald, additional, Tietge, Uwe J.F., additional, Pabst, Oliver, additional, Grote, Karsten, additional, Drexler, Helmut, additional, Förster, Reinhold, additional, and Schieffer, Bernhard, additional

Published
2010
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37. Acute perioperative-stress-induced increase of atherosclerotic plaque volume and vulnerability to rupture in apolipoprotein-E-deficient mice is amenable to statin treatment and IL-6 inhibition

Author

Janssen, Henrike, Wagner, Christian S., Demmer, Philipp, Callies, Simone, Sölter, Gesine, Loghmani-khouzani, Houra, Hu, Niandan, Schuett, Harald, Tietge, Uwe J. F., Warnecke, Gregor, Larmann, Jan, and Theilmeier, Gregor

Abstract

Myocardial infarction and stroke are frequent after surgical procedures and consume a considerable amount of benefit of surgical therapy. Perioperative stress, induced by surgery, is composed of hemodynamic and inflammatory reactions. The effects of perioperative stress on atherosclerotic plaques are ill-defined. Murine models to investigate the influence of perioperative stress on plaque stability and rupture are not available. We developed a model to investigate the influence of perioperative stress on plaque growth and stability by exposing apolipoprotein-E-deficient mice, fed a high cholesterol diet for 7 weeks, to a double hit consisting of 30 min of laparotomy combined with a substantial blood loss (approximately 20% of total blood volume; 400 µl). The innominate artery was harvested 72 h after the intervention. Control groups were sham and baseline controls. Interleukin-6 (IL-6) and serum amyloid A (SAA) plasma levels were determined. Plaque load, vascular smooth muscle cell (VSMC) and macrophage content were quantified. Plaque stability was assessed using the Stary score and frequency of signs of plaque rupture were assessed. High-dose atorvastatin (80 mg/kg body weight/day) was administered for 6 days starting 3 days prior to the double hit. A single dose of an IL-6-neutralizing antibody or the fusion protein gp130-Fc selectively targeting IL-6 trans-signaling was subcutaneously injected. IL-6 plasma levels increased, peaking at 6 h after the intervention. SAA levels peaked at 24 h (n=4, P<0.01). Plaque volume increased significantly with the double hit compared to sham (n=8, P<0.01). More plaques were scored as complex or bearing signs of rupture after the double hit compared to sham (n=5-8, P<0.05). Relative VSMC and macrophage content remained unchanged. IL-6-inhibition or atorvastatin, but not blocking of IL-6 trans-signaling, significantly decreased plaque volume and complexity (n=8, P<0.01). Using this model, researchers will be able to further investigate the pathophysiology of perioperative plaque stability, which can result in myocardial infarction, and, additionally, to test potential protective strategies.

Published
2015
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38. Suppressor of Cytokine Signaling 1 is Involved in Gene Regulation Which Controls the Survival of Ly6C low Monocytes in Mice.

Author

Schuett J, Kreutz J, Grote K, Vlacil AK, Schuett H, Oberoi R, Schmid A, Witten A, Stoll M, Schieffer B, and Rühle F

Subjects
Animals, Atherosclerosis genetics, Atherosclerosis pathology, Cell Survival, Mice, Mice, Knockout, Monocytes pathology, Suppressor of Cytokine Signaling 1 Protein genetics, Antigens, Ly, Atherosclerosis metabolism, Gene Expression Regulation, Monocytes metabolism, Suppressor of Cytokine Signaling 1 Protein metabolism
Abstract

Background/aims: Inflammatory processes are controlled by the fine-tuned balance of monocyte subsets. In mice, different subsets of monocytes can be distinguished by the expression of Ly6C that is highly expressed on inflammatory monocytes (Ly6C high ) and to a lesser extent on patrolling monocytes (Ly6C low ). Our previous study revealed an accumulation of Ly6C high monocytes in atherosclerotic-prone mice bearing a deficiency in suppressor of cytokine signaling (SOCS)-1 leading to an increased atherosclerotic burden. To decipher the underlying mechanisms, we performed a genome-wide analysis of SOCS-1-dependent gene regulation in Ly6C high and Ly6C low monocytes., Methods: In monocyte subsets from SOCS-1competent and -deficient mice differentially regulated genes were identified using an Illumina mRNA microarray (45,200 transcripts), which were randomly validated by qPCR. Principal component analysis was performed to further characterize mRNA profiles in monocyte subsets. To unravel potential regulatory mechanisms behind the differential mRNA expression, in silico analysis of a transcription factor (TF) network correlating with SOCS-1-dependent mRNA expression was carried out and combined with a weighted correlation network analysis (WGCNA)., Results: mRNA analysis in monocyte subsets revealed 46 differentially regulated genes by 2-fold or more. Principal component analysis illustrated a distinct separation of mRNA profiles in monocyte subsets from SOCS-1-deficient mice. Notably, two cell surface receptors crucially involved in the determination of monocyte differentiation and survival, C-X3-C chemokine receptor 1 (CX3CR1) and colony stimulating factor 1 receptor (CSF1R), were identified to be regulated by SOCS-1. Moreover, in silico analysis of a TF network in combination with the WGCNA revealed genes coding for PPAR-γ, NUR77 and several ETSdomain proteins that act as pivotal inflammatory regulators., Conclusion: Our study reveals that SOCS-1 is implicated in a TF network regulating the expression of central transcription factors like PPAR-γ and NUR77 thereby influencing the expression of CX3CR1 and CSF1R that are known to be pivotal for the survival of Ly6C low monocytes., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© Copyright by the Author(s). Published by Cell Physiol Biochem Press.)

Published
2019
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