0000000000004673

AUTHOR

Tilo Grosser

0000-0001-8569-8396

showing 4 related works from this author

Highly efficient liposome-mediated gene transfer of inducible nitric oxide synthase in vivo and in vitro in vascular smooth muscle cells.

2000

Objective: The efficient introduction of regulatory genes into vascular smooth muscle cells (SMCs) is one of the most promising options for gene therapy of cardiovascular diseases. Cationic liposome-mediated gene transfer may become a favorable transfection technique with regard to patient’s safety for in vivo administration. However, this method until now has its limitation in a low transfection efficiency. Therefore, the present study was designed to improve cationic liposome-mediated transfection of rabbit vascular SMCs in vitro and in vivo, in order to enhance transfection efficiency and present an optimized system which may offer a potential therapeutic benefit for in vivo application.…

LipopolysaccharidesMalePathologymedicine.medical_specialtyVascular smooth musclePhysiologyTransgeneGenetic enhancementBlotting WesternGenetic VectorsGene ExpressionNitric Oxide Synthase Type IIApoptosisCoronary DiseaseBiologyMuscle Smooth VascularIn vivoPhysiology (medical)Culture TechniquesmedicineCell AdhesionAnimalsHumansRegulator geneReporter geneReverse Transcriptase Polymerase Chain ReactionGenetic transferGene Transfer TechniquesTransfectionGenetic TherapyFlow CytometryCell biologyRabbitsNitric Oxide SynthaseCardiology and Cardiovascular MedicineCell DivisionCardiovascular research
researchProduct

Involvement of PKC and NF-κB in Nitric Oxide Induced Apoptosis in Human Coronary Artery Smooth Muscle Cells

2001

Apoptosis of vascular smooth muscle cells is critically involved in progression of atherosclerosis and may prevent intimal hyperplasia in restenosis and vascular remodeling. Nitric oxide (NO) is known to induce apoptosis, but the signaling pathways still remain unclear. We investigated p53 accumulation, protein kinase C (PKC) activation and nuclear transcription factor (NF-kappaB) binding activity as possible signaling mechanisms of NO-induced apoptosis. Apoptosis was induced dose-dependently with the NO-donors sodiumnitroprusside (SNP: 232+/-48%) and SIN-1 (241+/-90% of actinomycin D induced apoptosis; means +/- SEM, *por =0.05 vs. control) in HSMC. Inhibition of PKC significantly attenuat…

Nitroprussidemedicine.medical_specialtyVascular smooth muscleIntimal hyperplasiaPhysiologyApoptosisDNA FragmentationNaphthalenesNitric OxideMuscle Smooth VascularNitric oxidechemistry.chemical_compoundNF-KappaB Inhibitor alphaRestenosisInternal medicinemedicineHumansNitric Oxide DonorsEnzyme InhibitorsCells CulturedProtein Kinase CProtein kinase CCell Nucleusbusiness.industryNF-kappa BNF-κBStaurosporinemedicine.diseaseCoronary VesselsDNA-Binding Proteinsmedicine.anatomical_structurechemistryApoptosisMolsidomineCancer researchCardiologyI-kappa B ProteinsTumor Suppressor Protein p53businessArteryCellular Physiology and Biochemistry
researchProduct

NO Reduces PMN Adhesion to Human Vascular Endothelial Cells Due to Downregulation of ICAM-1 mRNA and Surface Expression

2000

Reperfusion damage is largely due to the adherence of polymorphonuclear leukocytes to the endothelium initiated by adhesion molecule upregulation. The reduced endothelial nitric oxide release during ischemia may be involved in the upregulation of intercellular adhesion molecule 1. In this study, we tested if nitric oxide donors suppress polymorphonuclear leukocyte adherence to activated endothelial cells by inhibition of the intercellular adhesion molecule 1 surface expression. Confluent human umbilical vein endothelial cells were stimulated with tumor necrosis factor alpha (300 U/mL) after preincubation with increasing concentrations of the nitric oxide donors CAS 1609 (0.005-5 mM/L) and 3…

AdultUmbilical VeinsEndotheliumNeutrophilsIntercellular Adhesion Molecule-1Cell Culture TechniquesDown-RegulationNitric Oxide Synthase Type IINitric OxideTransfectionUmbilical veinNitric oxidechemistry.chemical_compoundmedicineCell AdhesionHumansSaphenous VeinRNA MessengerICAM-1biologyTumor Necrosis Factor-alphaMembrane ProteinsHematologyIntercellular Adhesion Molecule-1Molecular biologyEndothelial stem cellNitric oxide synthasemedicine.anatomical_structurechemistryBiochemistryGene Expression Regulationbiology.proteinTumor necrosis factor alphaEndothelium VascularNitric Oxide Synthase
researchProduct

Lokale Medikamentengabe und Gentherapie

1997

Eines der wichtigsten Probleme der klinischen Kardiologie, die Entwickung einer Restenose nach koronarer Ballonangioplastie, ist bisher noch nicht befriedigend gelöst. Die pathophysiologischen Erkenntnisse über die Mechanismen der Neointimabildung sind noch unvollständig, und zahlreiche Therapiestudien mit systemisch applizierten Pharmaka mit unterschiedlichem Wirkungsmechanismus sind fehlgeschlagen. Mögliche innovative Therapieansätze betreffen die hochdosierte lokale Substanzapplikation an der Dilatationsstelle und lokale gentherapeutische Eingriffe zur Verhinderung der Neointimabildung durch Proliferationshemmung der glatten Gefäßmuskelzellen. Zahlreiche Kathetermodelle sind entwickelt w…

Gynecologymedicine.medical_specialtybusiness.industryMedicineGene transferCardiology and Cardiovascular MedicinebusinessHerz
researchProduct