0000000000024835

AUTHOR

S.-y. Weng

showing 7 related works from this author

P0431 : IL-4/IL-13 exacerbate liver fibrosis progression through alternatively activated macrophages

2015

Hepatologybusiness.industryLiver fibrosisInterleukin 13ImmunologyMedicinebusinessInterleukin 4Journal of Hepatology
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P0311 : Balb/c and C57/Bl6 mice exhibit differences in their susceptibility and anti-tumor response to B16F10 melanoma liver metastasis

2015

Antitumor activityC57 bl6 miceHepatologybiologybusiness.industryCancer researchMedicineB16f10 melanomabusinessbiology.organism_classificationmedicine.diseaseBALB/cMetastasisJournal of Hepatology
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Inducible knockdown of procollagen I protects mice from liver fibrosis and leads to dysregulated matrix genes and attenuated inflammation.

2017

Organ fibrosis is characterized by a chronic wound-healing response, with excess deposition of extracellular matrix components. Here, collagen type I represents the most abundant scar component and a primary target for antifibrotic therapies. Liver fibrosis can progress to cirrhosis and primary liver cancer, which are the major causes of liver related morbidity and mortality. However, a (pro-)collagen type I specific therapy remains difficult and its therapeutic abrogation may incur unwanted side effects. We therefore designed tetracycline-regulated procollagen alpha1(I) short hairpin (sh)RNA expressing mice that permit a highly efficient inducible knockdown of the procollagen alpha1(I) gen…

0301 basic medicineGenetically modified mouseLiver CirrhosisPathologymedicine.medical_specialtyCirrhosisInflammationMice TransgenicCollagen Type ISmall hairpin RNAExtracellular matrix03 medical and health sciencesMiceFibrosismedicineAnimalsRNA Small InterferingMolecular BiologyCells CulturedGene knockdownExtracellular Matrix ProteinsChemistryMouse Embryonic Stem CellsFibroblastsmedicine.diseaseProcollagen peptidaseDisease Models Animal030104 developmental biologyGene Expression RegulationGene Knockdown TechniquesCancer researchmedicine.symptomProcollagenMatrix biology : journal of the International Society for Matrix Biology
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P0455 : IL-4Ra oegulates liver fibrosis differently during progression and reversal phases by modulating the ratio of M1 vs M2 macrophages

2015

Hepatologybusiness.industryLiver fibrosisImmunologyMedicinebusinessJournal of Hepatology
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AMPK regulates macrophage polarization in adipose tissue inflammation and NASH

2013

Molecular and Translational Medicine, Dept. of Medicine I, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrase 1,55116 Mainz, GermanyCOMMENTARY ON:Hematopoietic AMPK beta1 reduces mouse adipose tissue mac-rophage inflammation and insulin resistance in obesity. Galic S,Fullerton MD, Schertzer JD, Sikkema S, Marcinko K, Walkley CR,Izon D, Honeyman J, Chen ZP, van Denderen BJ, Kemp BE, Stein-berg GR. J Clin Invest 2011;121(12):4903–15. Copyright 2011.Reprinted with permission of American Society for ClinicalInvestigation.http://www.ncbi.nlm.nih.gov/pubmed/22080866Abstract: Individuals who are obese are frequently insulin resistant,putting them at increased risk of d…

AMPKmedicine.medical_specialtyMacrophageMacrophage polarizationAdipose tissueAdipose tissueM1M2Insulin resistanceInternal medicineNAFLDmedicineBeta oxidationchemistry.chemical_classificationHepatologybiologyGlucose transporterNASHFatty acidAMPKInsulin resistanceType 2 diabetesmedicine.diseaseFatty acidFibrosisEndocrinologychemistryLiverbiology.proteinGLUT4Research ArticleJournal of Hepatology
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Regulatory T cell deficient scurfy mice exhibit a Th2/M2-like inflammatory response in the skin

2017

Abstract Background Scurfy mice have a functional defect in regulatory T cells (Treg), which leads to lethal multi-organ inflammation. The missing Treg function results in uncontrolled autoimmune cellular and humoral inflammatory responses. We and others have previously shown that during the course of disease scurfy mice develop severe skin inflammation and autoantibodies including anti-nuclear autoantibodies (ANA). Objective Autoimmune skin inflammation and ANA are hallmarks for the diagnosis of autoimmune connective tissue diseases; therefore we analyzed scurfy mice for typical signs of these diseases. Methods Indirect immunofluorescence was used to specify the ANA pattern in scurfy mice.…

Male0301 basic medicinePathologymedicine.medical_specialtyRegulatory T cellCD3Fluorescent Antibody TechniqueConnective tissueDermatitisInflammationDermatologyT-Lymphocytes RegulatoryBiochemistrySclerodermaAutoimmune DiseasesMice03 medical and health sciencesMixed connective tissue diseaseFibrosismedicineAnimalsMolecular BiologySkinCell NucleusScleroderma SystemicTissue Inhibitor of Metalloproteinase-1biologybusiness.industryMacrophagesAutoantibodyForkhead Transcription FactorsMacrophage ActivationFlow Cytometrymedicine.diseaseFibrosisUp-Regulation030104 developmental biologymedicine.anatomical_structureAntibodies AntinuclearImmunologybiology.proteinCytokinesFemaleCollagenmedicine.symptombusinessJournal of Dermatological Science
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Gliptins Suppress Inflammatory Macrophage Activation to Mitigate Inflammation, Fibrosis, Oxidative Stress, and Vascular Dysfunction in Models of Nona…

2017

Abstract Aims: Nonalcoholic steatohepatitis (NASH) is characterized by steatosis, panlobular inflammation, liver fibrosis, and increased cardiovascular mortality. Dipeptidyl peptidase-4 inhibitors (gliptins) are indirect glucagon-like peptide 1 agonists with antidiabetic and anti-inflammatory activity, used for the treatment of type 2 diabetes. Their potential and underlying mechanisms to treat metabolic liver inflammation and fibrosis as well as the associated vascular dysfunction remain to be explored. Results: In the methionine/choline-deficient (MCD) diet and Mdr2−/− models of NASH and liver fibrosis, treatment with sitagliptin and linagliptin significantly decreased parameters of steat…

0301 basic medicinemedicine.medical_specialtyPhysiologyClinical BiochemistryAnti-Inflammatory AgentsGene ExpressionInflammationType 2 diabetes030204 cardiovascular system & hematologymedicine.disease_causeBiochemistryAntioxidantsProinflammatory cytokineMice03 medical and health sciences0302 clinical medicineNon-alcoholic Fatty Liver DiseaseFibrosisInternal medicinemedicineAnimalsMyeloid CellsMolecular BiologyDipeptidyl peptidase-4General Environmental ScienceInflammationMice KnockoutDipeptidyl-Peptidase IV Inhibitorsbusiness.industryMacrophagesCell BiologyMacrophage Activationmedicine.diseaseFibrosisDietDisease Models AnimalOxidative Stress030104 developmental biologyEndocrinologyLiverNADPH Oxidase 2General Earth and Planetary SciencesTumor necrosis factor alphaSteatosismedicine.symptomReactive Oxygen SpeciesbusinessBiomarkersOxidative stressAntioxidants & Redox Signaling
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