0000000000407832

AUTHOR

Giuseppina Milano

0000-0002-5560-4667

showing 2 related works from this author

Toll-like receptor 5 deficiency exacerbates cardiac injury and inflammation induced by myocardial ischaemia-reperfusion in the mouse

2015

Myocardial ischaemia-reperfusion (MIR) triggers a sterile inflammatory response important for myocardial healing, but which may also contribute to adverse ventricular remodelling. Such inflammation is initiated by molecular danger signals released by damaged myocardium, which induce innate immune responses by activating toll-like receptors (TLRs). Detrimental roles have been recently reported for TLR2, TLR3 and TLR4. The role of other TLRs is unknown. We therefore evaluated the role of TLR5, expressed at high level in the heart, in the development of myocardial damage and inflammation acutely triggered by MIR. TLR5−/− and wild-type (WT) mice were exposed to MIR (30 min ischaemia, 2 h reperf…

MaleChemokinemedicine.medical_specialtyGenotypep38 mitogen-activated protein kinasesMyocardial InfarctionMyocardial Reperfusion InjuryInflammation030204 cardiovascular system & hematologyBiologyp38 Mitogen-Activated Protein KinasesVentricular Function LeftProinflammatory cytokineVentricular Dysfunction Left03 medical and health sciences0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicinemedicineAnimalsPhosphorylationProtein kinase B030304 developmental biologyInflammationMice Knockout0303 health sciencesToll-like receptorMyocardiumGeneral MedicineImmunity Innate3. Good healthMice Inbred C57BLDisease Models AnimalOxidative StressToll-Like Receptor 5CXCL2PhenotypeEndocrinologybiology.proteinTLR4Inflammation Mediatorsmedicine.symptomProto-Oncogene Proteins c-aktClinical Science
researchProduct

Phosphodiesterase-5 Inhibition Alleviates Pulmonary Hypertension and Basal Lamina Thickening in Rats Challenged by Chronic Hypoxia

2018

javax.xml.bind.JAXBElement@6f8948ff Hypoxia represents both an outcome of cardiopulmonary diseases and a trigger for severe pulmonary complications as pulmonary hypertension. Because nitric oxide (NO) is a critical mediator in the development of pulmonary hypertension, the modulators of its downstream function may become target of pharmacological interventions aimed at alleviating the impact of this condition. Here, we investigate the effects of an early administration of phosphodiesterase-5 inhibitor in rats where pulmonary artery hypertension was induced by chronic exposure to hypoxia. javax.xml.bind.JAXBElement@162dc677 Rats were divided into three groups: normoxic control, hypoxic with …

0301 basic medicinemedicine.medical_specialtynitrites and nitratesPhysiologySildenafilsildenafil030204 cardiovascular system & hematologyphosphodiesterase 5lcsh:PhysiologyNitric oxideendothelial NO synthase; nitric oxide; nitrites and nitrates; phosphodiesterase 5; pulmonary hypertension; pulmonary vascular remodeling; right heart failure; sildenafil03 medical and health scienceschemistry.chemical_compound0302 clinical medicinenitric oxidePhysiology (medical)medicine.arteryInternal medicinepulmonary hypertensionmedicineendothelial NO synthaseOriginal ResearchCardiopulmonary diseaseLunglcsh:QP1-981business.industryright heart failureHypoxia (medical)medicine.diseasePulmonary hypertension030104 developmental biologymedicine.anatomical_structurechemistryVentriclePulmonary arteryCardiologymedicine.symptombusinesspulmonary vascular remodelingFrontiers in Physiology
researchProduct