A5082785538- Platelet Disorders and Treatments
- Blood groups and transfusion
- Antiplatelet Therapy and Cardiovascular Diseases
- Rheumatoid Arthritis Research and Therapies
- Heparin-Induced Thrombocytopenia and Thrombosis
- Blood disorders and treatments
- Galectins and Cancer Biology
- Retinoids in leukemia and cellular processes
- Toxin Mechanisms and Immunotoxins
- HER2/EGFR in Cancer Research
- Autoimmune Bullous Skin Diseases
- Axon Guidance and Neuronal Signaling
- Complement system in diseases
- Wnt/β-catenin signaling in development and cancer
- Autoimmune and Inflammatory Disorders Research
- Signaling Pathways in Disease
- NF-κB Signaling Pathways
- Cell Adhesion Molecules Research
- Peptidase Inhibition and Analysis
- Mesenchymal stem cell research
- Renal Diseases and Glomerulopathies
- Orthopedic Infections and Treatments
- Venous Thromboembolism Diagnosis and Management
- Bone Metabolism and Diseases
- Blood Coagulation and Thrombosis Mechanisms
Instituto de Investigación Sanitaria de Santiago
2018-2024
Servicio Gallego de Salud
2018-2024
Complejo Hospitalario Universitario de Santiago
2009-2022
Instituto de Investigación Biomédica de A Coruña
2011-2019
Complexo Hospitalario Universitario A Coruña
2009-2018
Center for Rheumatology
2017
Universidade de Santiago de Compostela
2009-2014
Universidade da Coruña
2014
Molecular diagnosis of patients with von Willebrand disease is pending in most populations due to the complexity and high cost conventional molecular analyses. The need for clinical characterization Spain prompted creation a multicenter project (PCM-EVW-ES) that resulted largest prospective cohort study all types disease. analysis relevant regions VWF, including intronic promoter regions, was achieved 556 individuals recruited via development simple, innovative, relatively low-cost protocol...
The diagnosis of von Willebrand disease (VWD) remains difficult in a significant proportion patients. A Spanish multicentre study investigated cohort 556 patients from 330 families who were analysed centrally. VWD was confirmed 480. Next generation sequencing (NGS) the whole coding VWF carried out all recruited patients, compared with phenotype, and final established. total 238 different mutations found, 154 not included Leiden Open Variation Database (LOVD). Of 463 found to have mutation/s....
We hypothesized that WNT5A could contribute to the enhanced migration and invasiveness of rheumatoid arthritis fibroblast-like synoviocytes (RA FLS), which is one incompletely understood aspects RA FLS aggressive phenotype. This hypothesis based on previous evidence a role in both, cell migration. Migration invasion were assessed after incubation with recombinant Wnt5a (rWnt5a) or silencing endogenous expression. The expression WNT5A, WNT receptors, cytokines, chemokines metalloproteinases...
Diagnostics of von Willebrand disease (VWD) includes assessment factor VIII (FVIII) coagulant activity, (VWF) antigen (VWF:Ag) and VWF ristocetin cofactor activity (VWF:RCo), more specific tests as multimeric genetic analyses are necessary for the correct VWD classification. The ACL AcuStar analyzer introduces chemiluminescence (CL) technology in detection with automated VWF:Ag VWF:RCo assays. Compare VWF:Ag-ELISA by aggregometry conventional assays new CL VWF:Ag-IL VWF:RCo-IL assays,...
Semaphorin 3B (Sema3B) decreases the migratory and invasive capacities of fibroblast-like synoviocytes (FLS) in rheumatoid arthritis (RA) suppresses expression matrix metalloproteinases. We undertook this study to examine role Sema3B a mouse model its RA patients.Clinical responses, histologic features, FLS function were examined wild-type (WT) Sema3B-/- mice K/BxN serum transfer arthritis. Protein messenger RNA joints murine FLS, as well synovial tissue from patients with arthralgia RA, was...
Rheumatoid arthritis (RA) is a common chronic inflammatory disease affecting primarily peripheral joints, which only partially controlled with current treatments. RA leads to pain, disability, deformities, and life expectancy shortening. Its pathogenesis complex involving multiple cell types signaling pathways that we incompletely understand. One of the have elucidated starts WNT5A contributes aggressive phenotype synoviocytes through RYK-RhoA/ROCK signaling. Now, explored contribution ROCK...
Large studies in von Willebrand disease patients, including Spanish and Portuguese registries, led to the identification of >250 different mutations. It is a challenge determine pathogenic effect potential splice site mutations on VWF mRNA. This study aimed elucidate true effects 18 mRNA processing, investigate contribution next-generation sequencing vivo disease, compare findings with silico prediction. RNA extracted from patient platelets leukocytes was amplified by RT-PCR sequenced using...
Background: Of patients with severe aortic stenosis, 15–25% present bleeding episodes possibly attributable to acquired von Willebrand syndrome (AVWS). AVWS associated mitral valve prosthesis leakage has not been reported. Methods and Results: Five receiving appropriate oral anticoagulation showed episodes; all of them required hospitalization two blood transfusions, a factor (VWF) analysis was performed. Two normal functioning metallic valves were included as controls. Before surgery, after...
Fibroblast-like synoviocytes (FLSs) are pivotal in inflammation and joint damage of rheumatoid arthritis (RA). They acquire an active aggressive phenotype, displaying increased migration invasiveness contributing to perpetuate synovial destruction cartilage bone. The main current therapies RA focused against inflammatory factors immune cells; however, a significant percentage patients do not successfully respond. Combined treatments with drugs that control reverse the pathogenic phenotype...
Background Mutation C1149R in the von Willebrand factor (VWF) gene has been thought to cause autosomal dominant severe type 1 disease (VWD).Design and Methods Eight patients from three unrelated families with this mutation were included present study who had distinct VWF abnormalities, not described earlier studies.Results The showed notably low levels of antigen (VWF:Ag), ristocetin cofactor activity (VWF:RCo), collagen binding (VWF:CB), a reduced ristocetin-induced platelet aggregation...
Abstract Objective Class 3 semaphorins are reduced in the synovial tissue of RA patients and these proteins involved pathogenesis disease. The aim this study was to identify transcription factors expression class synovium patients. Methods Protein mRNA from individuals at risk (IAR) patients, human umbilical vein endothelial cells (HUVEC) fibroblast-like synoviocytes (FLS) determined by ELISA, immunoblotting quantitative PCR. TCF-3, EBF-1 HOXA5 knocked down using siRNA. Cell viability,...
Abstract Rheumatoid arthritis (RA) is a systemic autoimmune disease including synovitis and synovial hyperplasia that contribute to joint destruction. Pivotal pathogenic mechanisms in this process are the dysregulated proliferation apoptosis of fibroblast-like synoviocytes (FLS). Unfortunately, FLS dysregulation not completely elucidated. Here, we explored new hypothesis based potent anti-proliferative pro-apoptotic activity retinoids some types cancer. Specifically, investigated role...
The multimeric analysis (MA) of plasma von Willebrand factor (VWF) evaluates structural integrity and helps in the diagnosis disease (VWD). This assay is a matter controversy, being considered by some investigators cumbersome only slightly informative. centralised study 'Molecular Clinical Profile Disease Spain (PCM-EVW-ES)' has been carried out including phenotypic assessment genetic next generation sequencing (NGS) VWF gene (VWF). aim present was to evaluate role MA these patients their...
Abstract: The correct diagnosis and classification of von Willebrand disease (VWD) is difficult because the variability its clinical expression limitations laboratory methods. However, correctly diagnosing VWD important for therapy genetic counselling. A survey related to referred patients in Spain revealed local diagnostic problems at least one third cases VWD. Consequently, a Spanish multicenter study was carried out which cohort 556 from 330 families analyzed centrally. confirmed 480...
Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovial hyperplasia and cartilage/bone destruction with systemic comorbidities. Despite advances in understanding the aetiology of RA novel biologic drugs, a substantial number individuals remain intolerant or resistant to these therapies. In this context, mesenchymal stem/stromal cell (MSC)-based therapy has emerged as innovative therapeutic alternative address unresolved treatment issues for patients thanks...
<h3>Background</h3> Fibroblast-like synoviocytes (FLS) are pivotal in inflammation and joint damage of rheumatoid arthritis (RA). These cells proliferate, become resistant to apoptosis, migrate invade, contributing perpetuate synovial destruction cartilage bone. Current treatments RA focused against inflammatory factors immune cells, however, a significant percentage patients do not successfully respond. Combined with drugs that control others reverse the pathogenic phenotype FLS could...
<h3>Background</h3> Fibroblast-like synoviocytes (FLS) are pivotal in the inflammation and joint damage of rheumatoid arthritis (RA). These cells acquire an aggressive phenotype; they migrate invade articular structures perpetuating synovial inflammation. Also, contribute to cartilage bone by secretion cytokines, metalloproteinases cathepsins. The mechanisms modulating migration invasion FLS not yet completely known. Recently, role non-canonical pathway Wnt5a has been highlighted these...