A5050620819- Congenital heart defects research
- Developmental Biology and Gene Regulation
- Blood properties and coagulation
- Cell Adhesion Molecules Research
- Cellular Mechanics and Interactions
- Erythrocyte Function and Pathophysiology
- Zebrafish Biomedical Research Applications
- Kruppel-like factors research
- Protein Tyrosine Phosphatases
- MicroRNA in disease regulation
- Cerebrovascular and genetic disorders
- Phagocytosis and Immune Regulation
- Signaling Pathways in Disease
- Angiogenesis and VEGF in Cancer
- Autophagy in Disease and Therapy
- Cytokine Signaling Pathways and Interactions
- Ubiquitin and proteasome pathways
- Invertebrate Immune Response Mechanisms
Insigneo
2019-2023
University of Sheffield
2019-2023
Centre for Life
2019
ABSTRACT Endothelial cell (EC) sensing of fluid shear stress direction is a critical determinant vascular health and disease. Unidirectional flow induces EC alignment homeostasis, whereas bidirectional has pathophysiological effects. ECs express several mechanoreceptors that respond to flow, but the mechanism for poorly understood. We determined, by using in vitro systems magnetic tweezers, β1 integrin key sensor force because it activated unidirectional, not bidirectional, shearing forces....
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...
Hemodynamic wall shear stress (WSS) exerted on the endothelium by flowing blood determines spatial distribution of atherosclerotic lesions. Disturbed flow (DF) with a low WSS magnitude and reversing direction promotes atherosclerosis regulating endothelial cell (EC) viability function, whereas un-DF which is unidirectional high atheroprotective. Here, we study role EVA1A (eva-1 homolog A), lysosome endoplasmic reticulum-associated protein linked to autophagy apoptosis, in WSS-regulated EC...
Atherosclerosis develops near branches and bends of arteries that are exposed to disturbed blood flow which exerts low wall shear stress (WSS). These mechanical conditions alter endothelial cells (EC) by priming them for inflammation inducing turnover. Homeobox (Hox) genes developmental involved in the patterning embryos along their anterior-posterior proximal-distal axes. Here we identified Hox regulated WSS investigated functions adult arteries.EC were isolated from inner (low WSS) outer...
ABSTRACT The ability of endothelial cells (EC) to sense blood flow direction is a critical determinant vascular health and disease. Unidirectional induces EC alignment homeostasis, whereas bidirectional has pathophysiological effects. express several mechanoreceptors that can respond fluid (shear stress) but the mechanism for sensing shearing force poorly understood. We observed using in vitro systems magnetic tweezers β1 integrin key sensor because it activated by unidirectional not forces....
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> Atherosclerosis is a chronic inflammatory disease marked by hardening and thickening of the arteries. The develops predominantly at arterial branches bends. These atheroprone areas are subjected to disturbed blood flow, which generates low oscillatory wall shear stress (LOSS), frictional force exerted on endothelial cells (EC). LOSS increases EC activation drives endothelial-to-mesenchymal transition (EndoMT), promotes atherosclerosis. molecular basis responses not...