0000000000142580

AUTHOR

Tanja Schönfelder

showing 4 related works from this author

Deep vein thrombus formation induced by flow reduction in mice is determined by venous side branches.

2013

Interaction between vascular wall abnormalities, inflammatory leukocytes, platelets, coagulation factors and hemorheology in the pathogenesis of deep vein thrombosis (DVT) is incompletely understood, requiring well defined animal models of human disease. METHODS AND RESULTS: We subjected male C57BL/6 mice to ligation of the inferior vena cava (IVC) as a flow reduction model to induce DVT. Thrombus size and weight were analyzed macroscopically and sonographically by B-mode, pulse wave (pw) Doppler and power Doppler imaging (PDI) using high frequency ultrasound. Thrombus size varied substantially between individual procedures and mice, irrespective of the flow reduction achieved by the ligatu…

Malemedicine.medical_specialtyPhysiologymedicine.medical_treatmentDeep veinVena Cava InferiorInferior vena cavaMicePhysiology (medical)Internal medicineOcclusionmedicineAnimalscardiovascular diseasesThrombusLigatureVenous Thrombosisbusiness.industryHematologymedicine.diseaseThrombosisMice Inbred C57BLDisease Models Animalmedicine.anatomical_structuremedicine.veincardiovascular systemCardiologyHemorheologyRadiologyCardiology and Cardiovascular MedicineLigationbusinessBlood Flow VelocityClinical hemorheology and microcirculation
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Platelet-localized FXI promotes a vascular coagulation-inflammatory circuit in arterial hypertension

2017

Multicellular interactions of platelets, leukocytes, and the blood vessel wall support coagulation and precipitate arterial and venous thrombosis. High levels of angiotensin II cause arterial hypertension by a complex vascular inflammatory pathway that requires leukocyte recruitment and reactive oxygen species production and is followed by vascular dysfunction. We delineate a previously undescribed, proinflammatory coagulation-vascular circuit that is a major regulator of vascular tone, blood pressure, and endothelial function. In mice with angiotensin II-induced hypertension, tissue factor was up-regulated, as was thrombin-dependent endothelial cell vascular cellular adhesion molecule 1 ex…

Blood PlateletsMale0301 basic medicinemedicine.medical_specialtyMacrophage-1 AntigenVascular Cell Adhesion Molecule-1Blood Pressure030204 cardiovascular system & hematologyThromboplastinMice03 medical and health sciencesTissue factor0302 clinical medicineThrombinInternal medicinemedicineAnimalsHumansPlateletRats WistarEndothelial dysfunctionBlood CoagulationFactor XIAgedMice Knockoutbusiness.industryAngiotensin IIThrombinGeneral MedicineMiddle AgedOligonucleotides Antisensemedicine.diseaseAngiotensin IIMice Inbred C57BL030104 developmental biologyEndocrinologyBlood pressuremedicine.anatomical_structurePlatelet Glycoprotein GPIb-IX ComplexPathophysiology of hypertensionHypertensionFemalebusinessmedicine.drugBlood vesselScience Translational Medicine
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Innate Effector-Memory T-Cell Activation Regulates Post-Thrombotic Vein Wall Inflammation and Thrombus Resolution

2016

Rationale: Immune cells play an important role during the generation and resolution of thrombosis. T cells are powerful regulators of immune and nonimmune cell function, however, their role in sterile inflammation in venous thrombosis has not been systematically examined. Objective: This study investigated the recruitment, activation, and inflammatory activity of T cells in deep vein thrombosis and its consequences for venous thrombus resolution. Methods and Results: CD4 + and CD8 + T cells infiltrate the thrombus and vein wall rapidly on deep vein thrombosis induction and remain in the tissue throughout the thrombus resolution. In the vein wall, recruited T cells largely consist of effect…

CD4-Positive T-Lymphocytes0301 basic medicineChemokineMice 129 StrainPhysiologyMice TransgenicInflammationCD8-Positive T-Lymphocytes030204 cardiovascular system & hematologyVaricose VeinsMice03 medical and health sciences0302 clinical medicineImmune systemmedicineAnimalsHumansThrombusVeinInflammationVenous ThrombosisbiologyEffector Memory T-CellThrombosismedicine.diseaseThrombosisImmunity InnateCell biologyMice Inbred C57BLVenous thrombosis030104 developmental biologymedicine.anatomical_structureImmunologybiology.proteinmedicine.symptomCardiology and Cardiovascular MedicineCirculation Research
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Angiotensin II-induced vascular dysfunction depends on interferon-γ-driven immune cell recruitment and mutual activation of monocytes and NK-cells.

2013

Objective— Immune cells contribute to angiotensin II (ATII)–induced vascular dysfunction and inflammation. Interferon-γ (IFN-γ), an inflammatory cytokine exclusively produced by immune cells, seems to be involved in ATII-driven cardiovascular injury, but the actions and cellular source of IFN-γ remain incompletely understood. Approach and Results— IFN-γ −/− and Tbx21 −/− mice were partially protected from ATII-induced (1 mg/kg per day of ATII, infused subcutaneously by miniosmotic pumps) vascular endothelial and smooth muscle dysfunction, whereas mice overexpressing IFN-γ showed constitutive vascular dysfunction. Absence of T-box expressed in T cells (T-bet), the IFN-γ transcription factor…

Malemedicine.medical_specialtyAdoptive cell transfermedicine.medical_treatmentInflammationBiologyMonocytesInterferon-gammaMiceRandom AllocationImmune systemReference ValuesInternal medicinemedicineAnimalsVascular DiseasesVascular recruitmentVascular tissueAortaAngiotensin IIAngiotensin IIKiller Cells NaturalMice Inbred C57BLDisease Models AnimalOxidative StressCytokineEndocrinologyInterleukin 12Endothelium Vascularmedicine.symptomCardiology and Cardiovascular MedicineArteriosclerosis, thrombosis, and vascular biology
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