A5031727012- Heterotopic Ossification and Related Conditions
- Parathyroid Disorders and Treatments
- Medical Imaging and Pathology Studies
- TGF-β signaling in diseases
- Pulmonary Hypertension Research and Treatments
- HIV Research and Treatment
- Genetic Syndromes and Imprinting
- Congenital heart defects research
- HIV/AIDS drug development and treatment
- Renal and related cancers
- Bone Metabolism and Diseases
- Vascular Anomalies and Treatments
- Connective Tissue Growth Factor Research
- Pregnancy and preeclampsia studies
- Biomarkers in Disease Mechanisms
- Bioactive natural compounds
- Immune Cell Function and Interaction
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Cardiac Valve Diseases and Treatments
- Mesenchymal stem cell research
- Cardiac Fibrosis and Remodeling
- Ginseng Biological Effects and Applications
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Glioma Diagnosis and Treatment
- Dermatological and Skeletal Disorders
Nanomaterials and Nanotechnology Research Center
2023-2025
Leiden University
2015-2025
Consejo Superior de Investigaciones Científicas
2024-2025
Leiden University Medical Center
2015-2024
Gobierno del Principado de Asturias
2024
Loyola University Medical Center
2014-2022
Oncode Institute
2018-2020
Cancer Genomics Centre
2013-2017
University Hospital Münster
2016
Instituto de Investigación de Enfermedades Raras
2014
Endothelial-to-mesenchymal transition (EndMT) has been unveiled as a common cause for multitude of human pathologies, including cancer and cardiovascular disease. Vascular calcification is risk factor ischemic vascular disorders slowing may reduce mortality in affected patients. The absence early biomarkers hampers the identification patients at risk. EndMT are induced upon cooperation between distinct stimuli, inflammatory cytokines transforming growth beta (TGF-β) family members. However,...
Diffuse intrinsic pontine gliomas (DIPGs) are aggressive pediatric brain tumors for which there is currently no effective treatment. Some of these combine gain-of-function mutations in ACVR1, PIK3CA, and histone H3-encoding genes. The oncogenic mechanisms action ACVR1 unknown. Using mouse models, we demonstrate that Acvr1
The persistence of latent HIV-infected cellular reservoirs represents the major hurdle to virus eradication on patients treated with HAART. It has been suggested that successful depletion such will require a combination therapeutic agents can specifically and efficiently act cells harboring HIV-1 provirus. Using Jurkat-LAT-GFP cells, tractable model latency, we have found bryostatin-1 reactivates through classical PKC-dependent pathway. Bryostatin-1 also activates MAPKs NF-κB pathways...
AimsVascular calcification contributes to mortality and morbidity in atherosclerosis, chronic kidney disease, diabetes. Vascular calcific lesions contain osteoblast- chondroblast-like cells, suggesting a process of endochondral or membranous ossification thought result from the phenotypic plasticity vascular cells. Bone morphogenetic protein (BMP) signalling potentiates atherosclerotic calcification, whereas BMP inhibition attenuates inflammation atherogenic mice. We hypothesized endothelial...
Abstract Recent evidence has highlighted the role of endothelial‐to‐mesenchymal transition ( EndoMT ) in onset and progression a number human pathologies. involves loss an endothelial signature to generate unspecialized mesenchymal‐like cells, susceptible being re‐differentiated into mesodermal cell types, including osteoblasts, chondrocytes, adipocytes. Therefore, modulation molecular pathways controlling can be considered as therapeutic approach for particular diseases. In addition, may...
Background: Fibrodysplasia ossificans progressiva (FOP) is caused by an activating mutation (p.R206H) in the type I BMP receptor ALK2, leading to heterotopic ossification (HO) soft connective tissues. While aberrant Activin A-induced SMAD signaling central FOP pathogenesis, global alterations remain poorly understood. Methods: We performed phosphoproteomics, transcriptomics and biochemical analyses mesenchymal cells (MSCs) overexpressing wild-type ALK2-WT or mutant ALK2-R206H receptors...
Abstract Aims Precapillary pulmonary hypertension (precPH) results in increased right atrial (RA) stretch and pressure. The atrium is the major source of bone morphogenetic protein 10 (BMP10) adults, primarily produced by RA cardiomyocytes. aim this study was to investigate BMP10 expression heart systemic circulation identify potential triggers for secretion associated with precPH. Methods We examined mRNA expressions tissue. Circulating plasma levels were determined using ELISA....
Abstract Heterozygous mutations in the Bone morphogenetic protein (BMP) type I receptor ACVR1 , encoding activin-like kinase 2 (ALK2), underlie all cases of rare genetic musculoskeletal disorder Fibrodysplasia Ossificans Progressiva (FOP). The most commonly found mutant ALK2 p.R206H variant exhibits loss auto inhibition BMP signaling and can be activated by Activins, while wild-type receptors remain unresponsive. Consequently, downstream chondrogenic is enhanced, thus driving heterotopic...
The dietary phenolic curcumin (1a) is the archetypal network pharmacological agent, but characterized by an ill-defined pharmacophore. Nevertheless, structure–activity studies of 1a have mainly focused on a single biological end-point and structural element, aliphatic bis-enoyl moiety. comparative investigation more than one modification its aromatic region been largely overlooked. To address these issues, we investigated effect C-prenylation in three types curcuminoids, namely, itself (1a),...
Objective— Arterial calcification is considered a major cause of death and disabilities worldwide because the associated vascular remodeling leads to myocardial infarction, stroke, aneurysm, pulmonary embolism. This process occurs via poorly understood mechanisms involving variety cell types, intracellular mediators, extracellular cues within wall. An inverse correlation between endothelial primary cilia calcified areas has been described although signaling involved remain unknown. We aim...
ABSTRACT Fibrodysplasia ossificans progressiva (FOP) is an extremely rare congenital form of heterotopic ossification (HO), caused by heterozygous mutations in the activin A type I receptor (ACVR1), that encodes bone morphogenetic protein (BMP) ALK2. These enable ALK2 to induce downstream signaling response activins, thereby turning them into bone‐inducing agents. To date, there no cure for FOP. The further development FOP patient‐derived models may contribute discovery novel biomarkers and...
Endothelial-to-mesenchymal transition (EndMT) plays an important role in embryonic development and disease progression. Yet, how different members of the transforming growth factor-β (TGF-β) family regulate EndMT is not well understood. In current study, we report that TGF-β2, but bone morphogenetic protein (BMP)9, triggers murine endothelial MS-1 2H11 cells. TGF-β2 strongly upregulates transcription factor SNAIL, depletion Snail sufficient to abrogate TGF-β2-triggered mesenchymal-like cell...