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471 results on '"Krombach, Fritz"'

108. Vision on safe nanoparticles and nanotechnologies: Global and EU perspective. Nanosafety and REACH

Author

Savolainen, Kai, primary, Pylkkänen, Lea, additional, Norppa, Hannu, additional, Falck, Ghita, additional, Lindberg, Hanna, additional, Tuomi, Timo, additional, Vippola, Minnamari, additional, Alenius, Harri, additional, Brouwer, Derk, additional, Mark, Dave, additional, Bard, Delphine, additional, Berges, Markus, additional, Jankowska, Elzbieta, additional, Posniak, Malgorzata, additional, Farmer, Peter, additional, Singh, Raj, additional, and Krombach, Fritz, additional

Published
2008
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114. Effects of acute systemic administration of TiO 2 , ZnO, SiO 2 , and Ag nanoparticles on hemodynamics, hemostasis and leukocyte recruitment.

Author

Haberl, Nadine, Hirn, Stephanie, Holzer, Martin, Zuchtriegel, Gabriele, Rehberg, Markus, and Krombach, Fritz

Subjects
PHYSIOLOGICAL effects of nanoparticles, TITANIUM oxides, ZINC oxide, SILICON oxide, HEMODYNAMICS, HEMOSTASIS, LEUCOCYTES
Abstract

It has been suggested that engineered nanomaterials (ENM), once arrived in the circulation, may affect the cardiovascular system. The aim of thisin vivostudy was to screen major cardiovascular effects of acute systemic administration of a panel of five nanomaterials, TiO2anatase (NM-101), TiO2rutile (NM-104), ZnO (NM-110), SiO2(NM-200) and Ag (NM-300). Mice were anesthetized and the ENM were injected at a dose of 1 mg/kg via a catheter placed in the left femoral artery. Hemodynamic parameters were determined by invasive measurement of blood pressure and non-invasive measurement of heart rate. Ten minutes after injection of the ENM, the formation of light/dye-induced thrombi was assessed in the cremasteric microcirculation by intravital microscopy. In addition, the numbers of rolling, firmly adherent and transmigrated leukocytes were recorded in postcapillary cremasteric venules over a time period of 120 min after injection of ENM by intravital microscopy. The systemic administration of a single dose of the ENM tested did not dramatically alter hemodynamic parameters or affect early steps of leukocyte recruitment. However, the presence of circulating TiO2anatase, but not of TiO2rutile, SiO2, ZnO or Ag nanoparticles, significantly accelerated thrombus formation in the murine microcirculation. Moreover, TiO2anatase but not TiO2rutile nanoparticles increased murine platelet aggregationin vitro. Taken together, only one of the five systemically administered ENM, TiO2anatase, affected hemostasis, whereas none of the ENM tested in this screening study dramatically modulated hemodynamic parameters or early steps of leukocyte recruitment. [ABSTRACT FROM PUBLISHER]

Published
2015
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117. ESAM supports neutrophil extravasation, activation of Rho, and VEGF-induced vascular permeability

Author

Wegmann, Frank, primary, Petri, Björn, additional, Khandoga, Alexander Georg, additional, Moser, Christian, additional, Khandoga, Andrej, additional, Volkery, Stefan, additional, Li, Hang, additional, Nasdala, Ines, additional, Brandau, Oliver, additional, Fässler, Reinhard, additional, Butz, Stefan, additional, Krombach, Fritz, additional, and Vestweber, Dietmar, additional

Published
2006
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121. Delayed Chemokine Receptor 1 Blockade Prolongs Survival in Collagen 4A3–Deficient Mice with Alport Disease

Author

Ninichuk, Volha, primary, Gross, Oliver, additional, Reichel, Christoph, additional, Khandoga, Andrej, additional, Pawar, Rahul D., additional, Ciubar, Raluca, additional, Segerer, Stephan, additional, Belemezova, Emilia, additional, Radomska, Ewa, additional, Luckow, Bruno, additional, de Lema, Guillermo Perez, additional, Murphy, Philip M., additional, Gao, Ji-Liang, additional, Henger, Anna, additional, Kretzler, Matthias, additional, Horuk, Richard, additional, Weber, Manfred, additional, Krombach, Fritz, additional, Schlo[Combining Diaeresis]ndorff, Detlef, additional, and Anders, Hans-Joachim, additional

Published
2005
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122. Cardiovascular Effects of Fine and Ultrafine Particles

Author

Schulz, Holger, primary, Harder, Volker, additional, Ibald-Mulli, Angela, additional, Khandoga, Andrej, additional, Koenig, Wolfgang, additional, Krombach, Fritz, additional, Radykewicz, Roman, additional, Stampfl, Andreas, additional, Thorand, Barbara, additional, and Peters, Annette, additional

Published
2005
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146. Transient targeting of phosphoinositide 3-kinase acts as a roadblock in mast cells' route to allergy.

Author

Collmann, Emilie, Bohnacker, Thomas, Marone, Romina, Dawson, Janet, Rehberg, Markus, Stringer, Rowan, Krombach, Fritz, Burkhart, Christoph, Hirsch, Emilio, Hollingworth, Gregory J., Thomas, Matthew, and Wymann, Matthias P.

Abstract

Background: Tissue mast cell numbers are dynamically regulated by recruitment of progenitors from the vasculature. It is unclear whether progenitors are recruited during allergic sensitization and whether recruitment promotes allergic responses. Objective: We sought to (1) determine the effect of mast cell recruitment on acute allergic responses and (2) to define the role of phosphoinositide 3-kinase (PI3K) isoforms in sequential steps to allergic responses. Methods: Gene-targeted mice for PI3Kγ or PI3Kδ or mice treated with isoform-specific PI3K inhibitors (a novel PI3Kγ-specific inhibitor [NVS-PI3-4] and the PI3Kδ inhibitor IC87114) were used to monitor IgE-mediated mast cell recruitment, migration, adhesion by means of intravital microscopy, degranulation, TNF-α release, and subsequent endothelial cell activation in vivo or in bone marrow–derived mast cells. Results: Functional PI3Kγ, but not PI3Kδ, was crucial for mast cell accumulation in IgE-challenged skin, TNF-α release from IgE/antigen-stimulated mast cells, and mast cell/endothelial interactions and chemotaxis. PI3Kγ-deficient bone marrow–derived mast cells did not adhere to the endothelium in TNF-α–treated cremaster muscle, whereas PI3Kδ was not required. Depletion of TNF-α blocked IgE-induced mast cell recruitment, which links tissue mast cell–derived cytokine release to endothelial activation and mast cell recruitment. Interference with mast cell recruitment protected against anaphylaxis and was superior to blockage of tissue mast cell degranulation. Conclusions: Interference with mast cell recruitment to exacerbated tissues provides a novel strategy to alleviate allergic reactions and surpassed attenuation of tissue mast cell degranulation. This results in prolonged drug action and allows for reduction of drug doses required to block anaphylaxis, an important feature for drugs targeting inflammatory disease in general. [Copyright &y& Elsevier]

Published
2013
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150. Roscovitine blocks leukocyte extravasation by inhibition of cyclin-dependent kinases 5 and 9.

Author

Berberich, Nina, Uhl, Bernd, Joore, Jos, Schmerwitz, Ulrike K, Mayer, Bettina A, Reichel, Christoph A, Krombach, Fritz, Zahler, Stefan, Vollmar, Angelika M, Fürst, Robert, and Fürst, Robert

Subjects
CYCLIN-dependent kinases, LEUCOCYTES, APOPTOSIS, CELL communication, PROTEIN kinases, TUMOR necrosis factors, GENETIC transcription, THERAPEUTICS
Abstract

Background and Purpose: Roscovitine, a cyclin-dependent kinase (CDK) inhibitor that induces tumour cell death, is under evaluation as an anti-cancer drug. By triggering leukocyte apoptosis, roscovitine can also enhance the resolution of inflammation. Beyond death-inducing properties, we tested whether roscovitine affects leukocyte-endothelial cell interaction, a vital step in the onset of inflammation.Experimental Approach: Leukocyte-endothelial cell interactions were evaluated in venules of mouse cremaster muscle, using intravital microscopy. In primary human endothelial cells, we studied the influence of roscovitine on adhesion molecules and on the nuclear factor-κB (NF-κB) pathway. A cellular kinome array, in vitro CDK profiling and RNAi methods were used to identify targets of roscovitine.Key Results: In vivo, roscovitine attenuated the tumour necrosis factor-α (TNF-α)-induced leukocyte adherence to and transmigration through, the endothelium. In vitro, roscovitine strongly inhibited TNF-α-evoked expression of endothelial adhesion molecules (E-selectin, intercellular cell adhesion molecule, vascular cell adhesion molecule). Roscovitine blocked NF-κB-dependent gene transcription, but not the NF-κB activation cascade [inhibitor of κB (IκB) kinase activity, IκB-α degradation, p65 translocation]. Using a cellular kinome array and an in vitro CDK panel, we found that roscovitine inhibited protein kinase A, ribosomal S6 kinase and CDKs 2, 5, 7 and 9. Experiments using kinase inhibitors and siRNA showed that the decreased endothelial activation was due solely to blockade of CDK5 and CDK9 by roscovitine.Conclusions and Implications: Our study highlights a novel mode of action for roscovitine, preventing endothelial activation and leukocyte-endothelial cell interaction by inhibition of CDK5 and 9. This might expand its usage as a promising anti-inflammatory compound. [ABSTRACT FROM AUTHOR]

Published
2011
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