Search results for "Platelet"

showing 10 items of 786 documents

Early inflammatory players in cutanous fibrosis.

2017

Systemic sclerosis (SSc) is one of the most complex systemic autoimmune diseases with multi-organ involvement and heterogeneous clinical manifestations. The exact etiology of SSc is still unknown. However, identified target structures are components of endothelial cells, the innate/adaptive immune systems and fibroblasts, resulting in the hallmarks of the disease in form of inflammation/autoimmunity, vasculopathy and fibrosis of the skin and internal organs. There has been a large body of evidence that the adaptive immune system with autoreactive T and B cells producing autoantibodies plays a central role in the pathogenesis of SSc but the role of earlier pathogenic processes involving the …

0301 basic medicineInflammationAutoimmunityDermatologyBiologymedicine.disease_causeBiochemistryAutoimmunity03 medical and health sciences0302 clinical medicineImmune systemmedicineLeukocytesHumansPlatelet activationskin and connective tissue diseasesMolecular BiologyAutoantibodiesSkinAutoimmune diseaseInflammationImmunity CellularInnate immune systemScleroderma Systemicintegumentary systemInnate lymphoid cellEndothelial CellsFibroblastsmedicine.diseaseAcquired immune systemPlatelet ActivationFibrosisImmunity Innate030104 developmental biology030220 oncology & carcinogenesisImmunologymedicine.symptomImmunosuppressive AgentsJournal of dermatological science
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The Role of JAK/STAT Molecular Pathway in Vascular Remodeling Associated with Pulmonary Hypertension

2021

Pulmonary hypertension is defined as a group of diseases characterized by a progressive increase in pulmonary vascular resistance (PVR), which leads to right ventricular failure and premature death. There are multiple clinical manifestations that can be grouped into five different types. Pulmonary artery remodeling is a common feature in pulmonary hypertension (PH) characterized by endothelial dysfunction and smooth muscle pulmonary artery cell proliferation. The current treatments for PH are limited to vasodilatory agents that do not stop the progression of the disease. Therefore, there is a need for new agents that inhibit pulmonary artery remodeling targeting the main genetic, molecular,…

0301 basic medicineJanus kinase 2 (JAK2)QH301-705.5Hypertension PulmonaryInflammationReviewVascular Remodeling030204 cardiovascular system & hematologyModels BiologicalCatalysisstatInorganic Chemistry03 medical and health sciences0302 clinical medicinemedicine.arterymedicineAnimalsHumanssignal transducer and activator of transcription 3 (STAT3)pulmonary hypertension (PH)Physical and Theoretical ChemistryEndothelial dysfunctionBiology (General)Molecular BiologyQD1-999SpectroscopyJanus Kinasesbiologybusiness.industryOrganic ChemistryJAK-STAT signaling pathwayGeneral Medicinemedicine.diseasePulmonary hypertensionComputer Science ApplicationsSTAT Transcription FactorsChemistry030104 developmental biologyPulmonary arterybiology.proteinCancer researchmedicine.symptombusinessMyofibroblastPlatelet-derived growth factor receptorSignal TransductionInternational Journal of Molecular Sciences
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Pharmacokinetics of a sustained release formulation of PDGFβ-receptor directed carrier proteins to target the fibrotic liver

2018

Liver fibrogenesis is associated with excessive production of extracellular matrix by myofibroblasts that often leads to cirrhosis and consequently liver dysfunction and death. Novel protein-based antifibrotic drugs show high specificity and efficacy, but their use in the treatment of fibrosis causes a high burden for patients, since repetitive and long-term parenteral administration is required as most proteins and peptides are rapidly cleared from the circulation. Therefore, we developed biodegradable polymeric microspheres for the sustained release of proteinaceous drugs. We encapsulated the drug carrier pPB-HSA, which specifically binds to the PDGF beta R that is highly upregulated on a…

0301 basic medicineLiver CirrhosisMaleCirrhosisPolymersLiver fibrosisPharmaceutical Science02 engineering and technologyPharmacologyMULTIBLOCK-COPOLYMERReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesPharmacokineticsFibrosisIn vivomedicinein vitro in vivo correlationAnimalsControlled releaseFIBROSISBiodegradable polymeric microspheresDRUG-DELIVERYSerum AlbuminIN-VIVOMice KnockoutPOLYMERIC MICROSPHERESDrug CarriersINTERFERON-GAMMAChemistryProtein deliveryAlbuminPDGF beta-receptor targeted drug carrier021001 nanoscience & nanotechnologymedicine.diseaseControlled releaseIMPLANTSMicrospheresANTIFIBROTIC THERAPIESMice Inbred C57BLMICE030104 developmental biologyDelayed-Action PreparationsDrug delivery0210 nano-technologyDrug carrierGROWTH-FACTOR RECEPTOR
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Imatinib spares cKit-expressing prostate neuroendocrine tumors, whereas kills seminal vesicle epithelial-stromal tumors by targeting PDGFR-β

2017

Abstract Prostate cancer is a leading cause of cancer-related death in males worldwide. Indeed, advanced and metastatic disease characterized by androgen resistance and often associated with neuroendocrine (NE) differentiation remains incurable. Using the spontaneous prostate cancer TRAMP model, we have shown that mast cells (MCs) support in vivo the growth of prostate adenocarcinoma, whereas their genetic or pharmacologic targeting favors prostate NE cancer arousal. Aiming at simultaneously targeting prostate NE tumor cells and MCs, both expressing the cKit tyrosine kinase receptor, we have tested the therapeutic effect of imatinib in TRAMP mice. Imatinib-treated TRAMP mice experience a pa…

0301 basic medicineMaleCancer ResearchReceptor tyrosine kinaseAntineoplastic AgentProstate cancerMice0302 clinical medicineProstatebiologySeminal VesiclesImmunohistochemistryGene Expression Regulation NeoplasticNeuroendocrine TumorsProto-Oncogene Proteins c-kitmedicine.anatomical_structureOncology030220 oncology & carcinogenesisImatinib MesylateFemaleNeuroendocrine Tumormedicine.drugTrampHumanSignal TransductionPCA3medicine.medical_specialtyStromal cellXenograft Model Antitumor AssayProtein Kinase InhibitorAntineoplastic AgentsMice TransgenicReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesInternal medicineSeminal VesiclemedicineAnimalsHumansProtein Kinase InhibitorsAnimalProstatic NeoplasmsImatinibBiomarkermedicine.diseaseXenograft Model Antitumor AssaysDisease Models Animal030104 developmental biologyEndocrinologyImatinib mesylateProstatic Neoplasmbiology.proteinCancer researchBiomarkers
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The Commensal Microbiota Enhances ADP-Triggered Integrin αIIbβ3 Activation and von Willebrand Factor-Mediated Platelet Deposition to Type I Collagen

2020

The commensal microbiota is a recognized enhancer of arterial thrombus growth. While several studies have demonstrated the prothrombotic role of the gut microbiota, the molecular mechanisms promoting arterial thrombus growth are still under debate. Here, we demonstrate that germ-free (GF) mice, which from birth lack colonization with a gut microbiota, show diminished static deposition of washed platelets to type I collagen compared with their conventionally raised (CONV-R) counterparts. Flow cytometry experiments revealed that platelets from GF mice show diminished activation of the integrin αIIbβ3 (glycoprotein IIbIIIa) when activated by the platelet agonist adenosine diphosphate (ADP). Fu…

0301 basic medicineMaleGene Expression030204 cardiovascular system & hematologyvon Willebrand factorlcsh:Chemistrychemistry.chemical_compoundMice0302 clinical medicinePlateletToll-like receptor-2lcsh:QH301-705.5SpectroscopyMice KnockoutbiologyChemistryBrief ReportαIIbβ3General MedicineArteriesComputer Science ApplicationsCell biologyAdenosine DiphosphatePlatelet Glycoprotein GPIb-IX Complexgerm-freeplateletsFemaleType I collagenBlood PlateletsIntegrinPrimary Cell CulturePlatelet Glycoprotein GPIIb-IIIa ComplexCatalysisCollagen Type IInorganic Chemistry03 medical and health sciencesVon Willebrand factormedicineCell AdhesionmicrobiotaAnimalsGerm-Free LifeHumansPhysical and Theoretical ChemistryThrombusSymbiosisMolecular Biologyα<sub>IIb</sub>β<sub>3</sub>Innate immune systemOrganic ChemistryThrombosismedicine.diseaseImmunity InnateToll-Like Receptor 2Gastrointestinal MicrobiomeMice Inbred C57BLAdenosine diphosphateTLR2030104 developmental biologylcsh:Biology (General)lcsh:QD1-999biology.proteinInternational Journal of Molecular Sciences
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Plasmacytoid dendritic cells promote systemic sclerosis with a key role for TLR8

2018

Systemic sclerosis (SSc) is a multisystem life-threatening fibrosing disorder that lacks effective treatment. The link between the inflammation observed in organs such as the skin and profibrotic mechanisms is not well understood. The plasmacytoid dendritic cell (pDC) is a key cell type mediating Toll-like receptor (TLR)-induced inflammation in autoimmune disease patients, including lupus and skin diseases with interface dermatitis. However, the role of pDCs in fibrosis is less clear. We show that pDCs infiltrate the skin of SSc patients and are chronically activated, leading to secretion of interferon-α (IFN-α) and CXCL4, which are both hallmarks of the disease. We demonstrate that the s…

0301 basic medicineMaleInflammationPlasmacytoid dendritic cellPlatelet Factor 4SclerodermaArticlePathogenesis03 medical and health sciencesBleomycinMice0302 clinical medicineFibrosismedicineAnimalsHumansSkin030203 arthritis & rheumatologyAutoimmune diseaseSystemic lupus erythematosusScleroderma Systemicintegumentary systembusiness.industryMedicine (all)Interferon-alphahemic and immune systemsGeneral MedicineTLR7Dendritic CellsMiddle Agedmedicine.diseaseFibrosisDisease Models Animal030104 developmental biologyToll-Like Receptor 7Toll-Like Receptor 8ImmunologyFemalemedicine.symptombusinessSignal Transduction
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Combined platelet-rich plasma and lipofilling treatment provides great improvement in facial skin-induced lesion regeneration for scleroderma patient…

2017

Background The use of stem cells, including mesenchymal stem cells (MSCs), for regenerative medicine is gaining interest for the clinical benefits so far obtained in patients. This study investigates the use of adipose autologous tissue in combination with platelet-rich plasma (PRP) to improve the clinical outcome of patients affected by systemic sclerosis (SSc). Methods Adipose-derived mesenchymal stem cells (AD-MSCs) and PRPs were purified from healthy donors and SSc patients. The multilineage differentiation potential of AD-MSCs and their genotypic–phenotypic features were investigated. A cytokine production profile was evaluated on AD-MSCs and PRPs from both healthy subjects and SSc pat…

0301 basic medicineMalePathologyCell- and Tissue-Based TherapyAdipose tissueMedicine (miscellaneous)Gene ExpressionRegenerative MedicineCell therapyCell therapySystemic sclerosiAdipose-derived mesenchymal stem cells; Cell therapy; Lipofilling; Mesenchymal stem cells; Platelet-rich plasma; Regenerative medicine; Systemic sclerosis; Medicine (miscellaneous); Molecular Medicine; Biochemistry Genetics and Molecular Biology (miscellaneous); Cell Biologylcsh:QD415-436skin and connective tissue diseasesMesenchymal stem cellSkinAged 80 and overlcsh:R5-920integumentary systemCell DifferentiationStromal vascular fractionMiddle Agedmedicine.anatomical_structureAdipose TissueMolecular MedicineCytokinesSystemic sclerosisFemaleStem celllcsh:Medicine (General)Adultmedicine.medical_specialtyPrimary Cell CultureConnective tissueNeovascularization PhysiologicMesenchymal Stem Cell TransplantationBiochemistry Genetics and Molecular Biology (miscellaneous)lcsh:Biochemistry03 medical and health sciencesPlatelet-rich plasmaAntigens CDAdipose-derived mesenchymal stem cellsmedicineHumansCell ProliferationAdipose-derived mesenchymal stem cellLipofillingScleroderma Systemicbusiness.industryRegeneration (biology)ResearchMesenchymal stem cellMesenchymal Stem CellsCell Biology030104 developmental biologyPlatelet-rich plasmaImmunologybusinessStem cell researchtherapy
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Functional role of endothelial CXCL16/CXCR6-platelet-leucocyte axis in angiotensin II-associated metabolic disorders.

2018

Aims Angiotensin-II (Ang-II) is the main effector peptide of the renin-angiotensin system (RAS) and promotes leucocyte adhesion to the stimulated endothelium. Because RAS activation and Ang-II signalling are implicated in metabolic syndrome (MS) and abdominal aortic aneurysm (AAA), we investigated the effect of Ang-II on CXCL16 arterial expression, the underlying mechanisms, and the functional role of the CXCL16/CXCR6 axis in these cardiometabolic disorders. Methods and results Results from in vitro chamber assays revealed that CXCL16 neutralization significantly inhibited mononuclear leucocyte adhesion to arterial but not to venous endothelial cells. Flow cytometry and immunofluorescence s…

0301 basic medicineMaleRHOAPhysiologyMice Knockout ApoE030204 cardiovascular system & hematology0302 clinical medicineLeukocytesReceptorCells CulturedMetabolic SyndromebiologyChemistryAngiotensin IIMiddle AgedAortic AneurysmVascular endothelial growth factor ALosartanmedicine.anatomical_structurecardiovascular systemFemaleCardiology and Cardiovascular Medicinemedicine.drugSignal TransductionAdultBlood Plateletsmedicine.medical_specialtyEndothelium03 medical and health sciencesPhysiology (medical)Internal medicinemedicineCell AdhesionAnimalsHumansPlatelet activationReceptors CXCR6Angiotensin II receptor type 1Endothelial CellsChemokine CXCL16Platelet ActivationAngiotensin IICoculture TechniquesMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyCase-Control Studiesbiology.proteinAngiotensin II Type 1 Receptor BlockersCardiovascular research
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Ticagrelor, but not clopidogrel, reduces arterial thrombosis via endothelial tissue factor suppression

2017

The P2Y12 antagonist ticagrelor reduces mortality in patients with acute coronary syndrome (ACS), compared with clopidogrel, and the mechanisms underlying this effect are not clearly understood. Arterial thrombosis is the key event in ACS; however, direct vascular effects of either ticagrelor or clopidogrel with focus on arterial thrombosis and its key trigger tissue factor have not been previously investigated.Methods and results: Human aortic endothelial cells were treated with ticagrelor or clopidogrel active metabolite (CAM) and stimulated with tumour necrosis factor-alpha (TNF-α); effects on procoagulant tissue factor (TF) expression and activity, its counter-player TF pathway inhibito…

0301 basic medicineMaleTicagrelorAdenosineTime FactorsPhysiology030204 cardiovascular system & hematology2737 Physiology (medical)0302 clinical medicineP2Y12AntithromboticCells CulturedClopidogrelReceptors Purinergic P2Y123. Good healthClopidogrelmedicine.anatomical_structureCoagulation10209 Clinic for CardiologyCardiologyCardiology and Cardiovascular MedicineTicagrelormedicine.drugBlood PlateletsAcute coronary syndromemedicine.medical_specialtyProteasome Endopeptidase ComplexTiclopidineEndotheliumDown-Regulation610 Medicine & health2705 Cardiology and Cardiovascular MedicineThromboplastinEquilibrative Nucleoside Transporter 103 medical and health sciencesTissue factorFibrinolytic AgentsPhysiology (medical)Internal medicinemedicineAnimalsHumanscardiovascular diseasesBlood Coagulationbusiness.industryTumor Necrosis Factor-alphaEndothelial CellsThrombosis1314 Physiologymedicine.diseaseMice Inbred C57BLDisease Models Animal030104 developmental biologyProteolysisPurinergic P2Y Receptor AntagonistsbusinessCarotid Artery InjuriesPlatelet Aggregation Inhibitors
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Clinical Determinants of Thrombin Generation Measured in Presence and Absence of Platelets-Results from the Gutenberg Health Study.

2018

AbstractThe tendency of a plasma sample to generate thrombin, a central enzyme in blood coagulation, might be an important indicator of prothrombotic risk linked to cardiovascular disease (CVD), but the presence of platelets may be a critical determinant. Clinical data, laboratory markers and thrombin generation (TG), investigated in both platelet-rich plasma (PRP) and platelet-free plasma (PFP) at 1 pM TF, were available in 407 individuals from the Gutenberg Health Study. Given the well-known effect of anticoagulants on TG, subjects taking anticoagulants (n = 15) have been excluded resulting in 392 subjects for further analysis. Lag time, endogenous thrombin potential (ETP) and peak height…

0301 basic medicineMaleTime Factorspopulation030204 cardiovascular system & hematologyFibrinogenDISEASEHYPERCOAGULABILITYACTIVATION0302 clinical medicineRisk FactorsGermanyMedicinePlateletProspective StudiesBLOOD-COAGULATIONBlood coagulation testeducation.field_of_studybiologyPlatelet-Rich PlasmaMICROPARTICLESThrombinHematologyclinical epidemiologyMiddle AgedDEFICIENCYC-Reactive ProteinCoagulationCardiovascular Diseasesthrombin generationplateletsFemaleBlood Coagulation TestsMean Platelet Volumemedicine.drugAdultBlood Plateletsmedicine.medical_specialtyPopulationRisk AssessmentMECHANISMS03 medical and health sciencesThrombinINFLAMMATIONPredictive Value of TestsInternal medicineHumansMean platelet volumeeducationBlood CoagulationAgedVENOUS THROMBOEMBOLISMbusiness.industryPlatelet CountC-reactive proteinATHEROTHROMBOSIS030104 developmental biologyEndocrinologybiology.proteinbusinessThrombosis and haemostasis
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