A5081579448- SARS-CoV-2 and COVID-19 Research
- Immune cells in cancer
- Viral gastroenteritis research and epidemiology
- Animal Virus Infections Studies
- Angiogenesis and VEGF in Cancer
- Extracellular vesicles in disease
- Cell Adhesion Molecules Research
- Endoplasmic Reticulum Stress and Disease
- T-cell and B-cell Immunology
- Liver Disease Diagnosis and Treatment
- Phagocytosis and Immune Regulation
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Respiratory viral infections research
- Adenosine and Purinergic Signaling
- COVID-19 and Mental Health
- Animal Disease Management and Epidemiology
- Cancer Cells and Metastasis
- Inflammation biomarkers and pathways
- vaccines and immunoinformatics approaches
- Immunotherapy and Immune Responses
- Renal function and acid-base balance
- Developmental Biology and Gene Regulation
- Apelin-related biomedical research
- Kruppel-like factors research
- Vaccine Coverage and Hesitancy
University of Sheffield
2010-2022
Insigneo
2016-2022
Boston Children's Hospital
2016
Harvard University
2016
KU Leuven
2016
Imperial College London
2016
Erasmus University Rotterdam
2016
Royal Hallamshire Hospital
2010
Utrecht University
2004-2008
Blood flow influences atherosclerosis by generating wall shear stress, which alters endothelial cell (EC) physiology. Low stress induces dedifferentiation of EC through a process termed endothelial-to-mesenchymal transition (EndMT). The mechanisms underlying stress-regulation EndMT are uncertain. Here we investigated the role transcription factor Snail in low stress-induced EndMT. Studies cultured exposed to revealed that induced expression. Using gene silencing it was demonstrated...
Abstract Neutrophils are implicated in the pathogenesis of atherosclerosis but seldom detected atherosclerotic plaques. We investigated whether neutrophil-derived microvesicles may influence arterial pathophysiology. Here we report that levels circulating neutrophil enhanced by exposure to a high fat diet, known risk factor for atherosclerosis. Neutrophil accumulate at disease-prone regions arteries exposed disturbed flow patterns, and promote vascular inflammation murine model. Using...
Rationale: Blood flow–induced shear stress controls endothelial cell (EC) physiology during atherosclerosis via transcriptional mechanisms that are incompletely understood. The mechanosensitive transcription factor TWIST is expressed embryogenesis, but its role in EC responses to and focal unknown. Objective: To investigate whether regulates vascular dysfunction compare function development disease. Methods Results: expression of TWIST1 was studied both developing vasculature the initiation...
The processing and regulated secretion of IL-1beta are critical points control the biological activity this important pro-inflammatory cytokine. is produced by both monocytes macrophages, but rate mechanism release differ according to differentiation status origin these cells. We aimed study in human blood monocyte-derived macrophages. Toll-like receptor (TLR)-induced production were investigated for dependence upon caspase-1, P2X7 activation, loss membrane asymmetry associated with...
Endothelial cell (EC) sensing of disturbed blood flow triggers atherosclerosis, a disease arteries that causes heart attack and stroke, through poorly defined mechanisms. The Notch pathway plays central role in vessel growth homeostasis, but its potential has not been previously studied. Here, we show using porcine murine cultured human coronary artery EC activates the JAG1-NOTCH4 signaling pathway. Light-sheet imaging revealed enrichment JAG1 NOTCH4 atherosclerotic plaques, EC-specific...
Angiopoietins are a family of growth factors that ligands for the tyrosine kinase receptor, Tie2. Angiopoietin 1 (Ang-1) is agonistic Tie2, plays key role in blood vessel maturation and stability has been shown to possess anti-inflammatory properties. However, Tie2 expression demonstrated on human neutrophils observation migrate response Ang-1 vitro confounded research into its exact inflammation as well potential use therapeutic agent. We used mouse model peritoneal neutrophilic determine...
Abstract Neutrophils have been implicated in the pathogenesis of atherosclerosis, a lipid-driven disease arteries, but they are seldom found atherosclerotic plaques. To resolve this longstanding paradox, we investigated whether neutrophil-derived microvesicles may influence arterial pathophysiology. Clinical and pre-clinical studies revealed that levels circulating neutrophil were enhanced by exposure to high fat diet, known risk factor for atherosclerosis. Neutrophil accumulated at...
Abstract Endothelial cell (EC) sensing of fluid shear stress regulates atherosclerosis, a disease arteries that causes heart attack and stroke. Atherosclerosis preferentially develops at regions exposed to low oscillatory (LOSS), whereas high are protected. We show using inducible EC-specific genetic deletion in hyperlipidaemic mice the Notch ligands JAG1 DLL4 have opposing roles atherosclerosis. While endothelial Jag1 promoted atherosclerosis sites LOSS, Dll4 was atheroprotective. Analysis...
<h3>Introduction</h3> Mitogen activated protein kinase (MAPK) cascades are involved in the regulation of several cellular responses including migration or proliferation. We have shown previously that tribbles-1 (trb-1), a member tribbles family adaptor/scaffold proteins controls vascular smooth muscle proliferation and chemotaxis via direct interaction with JNK activator kinase, MKK4. However, regulatory role monocyte/macrophage function for members has also been reported. With current work,...
<h3>Introduction</h3> Genome wide association studies have identified Tribbles-1 (<i>TRIB1</i>) to be significantly associated with all major plasma lipid traits and as a risk factor for ischaemic heart disease myocardial infarction. Studies in mice using <i>Trib1</i> full body KO liver-specific over-expression models shown that hepatic expression of TRIB1 reduces circulating lipids. Additionally, has been implicated regulator alternatively activated macrophages. However the potential...