2015
Modulation of Sox10, HIF-1α, Survivin, and YAP by Minocycline in the Treatment of Neurodevelopmental Handicaps following Hypoxic Insult
Li Q, Tsuneki M, Krauthammer M, Couture R, Schwartz M, Madri JA. Modulation of Sox10, HIF-1α, Survivin, and YAP by Minocycline in the Treatment of Neurodevelopmental Handicaps following Hypoxic Insult. American Journal Of Pathology 2015, 185: 2364-2378. PMID: 26209807, PMCID: PMC5801488, DOI: 10.1016/j.ajpath.2015.05.016.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsApoptosisCell Cycle ProteinsDisease Models, AnimalHypoxiaHypoxia-Inducible Factor 1, alpha SubunitInhibitor of Apoptosis ProteinsMice, Inbred C57BLMinocyclineMultiple SclerosisPhosphoproteinsRepressor ProteinsSOXE Transcription FactorsSurvivinUp-RegulationYAP-Signaling ProteinsConceptsMinocycline treatmentNeurodevelopmental handicapHypoxic insultEffects of minocyclineUntoward side effectsAnimal model studiesPotential therapeutic targetSublethal hypoxic conditionsPremature infantsMultiple sclerosisCurrent therapiesTreatment trialsChronic hypoxiaSynaptic transmissionMurine modelMouse pupsMotor handicapNewborn populationSide effectsTherapeutic targetSublethal hypoxiaHIF-1αNerve transmissionMinocyclineCognitive functionDisturbed shear stress reduces Klf2 expression in arterial‐venous fistulae in vivo
Yamamoto K, Protack CD, Kuwahara G, Tsuneki M, Hashimoto T, Hall MR, Assi R, Brownson KE, Foster TR, Bai H, Wang M, Madri JA, Dardik A. Disturbed shear stress reduces Klf2 expression in arterial‐venous fistulae in vivo. Physiological Reports 2015, 3: e12348. PMID: 25780089, PMCID: PMC4393175, DOI: 10.14814/phy2.12348.Peer-Reviewed Original ResearchArteriovenous fistulaKLF2 expressionDisturbed shear stressFistula diameterMouse aortocaval fistula modelArterial-venous fistulaProtein expressionAortocaval fistula modelInferior vena cavaPotential therapeutic targetAVF maturationAVF patencyDuplex ultrasoundArterial inflowVena cavaVenous outflowArterial limbVenous limbFistula modelMouse modelArterial samplesFistulaTherapeutic targetWestern blotGauge needle
1995
Anti-C5 monoclonal antibody therapy prevents collagen-induced arthritis and ameliorates established disease.
Wang Y, Rollins S, Madri J, Matis L. Anti-C5 monoclonal antibody therapy prevents collagen-induced arthritis and ameliorates established disease. Proceedings Of The National Academy Of Sciences Of The United States Of America 1995, 92: 8955-8959. PMID: 7568051, PMCID: PMC41086, DOI: 10.1073/pnas.92.19.8955.Peer-Reviewed Original ResearchConceptsCollagen-induced arthritisRheumatoid arthritisComplement activationAnti-C5 mAbInflammatory joint diseaseOnset of arthritisMonoclonal antibody therapyTerminal complement activationAttractive therapeutic targetJoint inflammationAntibody therapySystemic administrationJoint diseaseNumerous disease statesImmunized animalsArthritisAnimal modelsTherapeutic targetPotent mediatorTerminal complement componentsActivated componentsComplement cascadeComplement componentsComplement systemMonoclonal antibodies