Search results for "11459 Center for Molecular Cardiology"

showing 2 items of 2 documents

An overview of the molecular mechanisms underlying development and progression of bicuspid aortic valve disease

2019

Bicuspid aortic valve (BAV) is a common congenital heart malformation frequently associated with the development of aortic valve diseases and severe aortopathy, such as aortic dilatation, aneurysm and dissection. To date, different genetic loci have been identified in syndromic and non- syndromic forms of BAV. Among these, genes involved in the regulation of extracellular matrix remodelling, epithelial to mesenchymal transition and nitric oxide metabolism appear to be the main contributors to BAV pathogenesis. However, no- single gene model explains BAV inheritance, suggesting that more factors are simultaneously involved. In this regard, characteristic epigenetic and immunological profiles…

0301 basic medicineaneurysm; aortic dilatation; aortic stenosis; aortopathy; bicuspid aortic valve; NOTCH1Aortic stenosibicuspid aortic valveHeart malformationAortic DiseasesHeart Valve Diseasesaortopathy610 Medicine & healthDisease030204 cardiovascular system & hematologyBioinformatics2705 Cardiology and Cardiovascular Medicine11459 Center for Molecular CardiologyPathogenesis03 medical and health sciences0302 clinical medicineAneurysmBicuspid aortic valveNOTCH1Bicuspid Aortic Valve Disease1312 Molecular BiologymedicineSettore MED/05 - Patologia ClinicaAnimalsHumansEpithelial–mesenchymal transitionEpigeneticsMolecular BiologyAortic dilatationbusiness.industryaortic stenosisaortic dilatationmedicine.disease030104 developmental biologyAortic ValveaneurysmDisease Progressioncardiovascular systemCardiology and Cardiovascular MedicinebusinessJournal of Molecular and Cellular Cardiology
researchProduct

Murine tissue factor disulfide mutation causes a bleeding phenotype with sex specific organ pathology and lethality.

2019

Tissue factor is highly expressed in sub-endothelial tissue. The extracellular allosteric disulfide bond Cys186-Cys209 of human tissue factor shows high evolutionary conservation and in vitro evidence suggests that it significantly contributes to tissue factor procoagulant activity. To investigate the role of this allosteric disulfide bond in vivo, we generated a C213G mutant tissue factor mouse by replacing Cys213 of the corresponding disulfide Cys190-Cys213 in murine tissue factor. A bleeding phenotype was prominent in homozygous C213G tissue factor mice. Pre-natal lethality of 1/3rd of homozygous offspring was observed between E9.5 and E14.5 associated with placental hemorrhages. After b…

Malemedicine.medical_specialtyOffspring610 Medicine & healthHemorrhage030204 cardiovascular system & hematologyBiologymedicine.disease_causeArticleThromboplastin11459 Center for Molecular Cardiology03 medical and health sciencesTissue factorArterial Thrombosis; Blood Coagulation and Fibrinolysis; Disorders of Coagulation and FibrinolysisMice0302 clinical medicineIn vivoPregnancyInternal medicinemedicineExtracellularAnimalsDisulfidesMutationHematologyPhenotypeIn vitroEndocrinologyPhenotype10036 Medical Clinic10076 Center for Integrative Human PhysiologyHemostasisMutation10209 Clinic for CardiologyFemale030215 immunologyHaematologica
researchProduct