DLL4 promotes partial endothelial-to-mesenchymal transition at atherosclerosis-prone regions of arteries.

Flowing blood regulates vascular development, homeostasis and disease by generating wall shear stress which has major effects on endothelial cell (EC) physiology. Low oscillatory shear stress (LOSS) induces a form of cell plasticity called endothelial-to-mesenchymal transition (EndMT). This process has divergent effects; in embryos LOSS-induced EndMT drives the development of atrioventricular valves, whereas in adult arteries it is associated with inflammation and atherosclerosis.

Green synthesis of mesoporous and biodegradable iron silicide nanoparticles for photothermal cancer therapy.

Photothermal nanomaterials have shown great potential for photothermal therapy. In this study, we developed a simple green method of magnesiothermic co-reduction for the synthesis of mesoporous, magnetic and biodegradable iron silicide nanoparticles (FeSi NPs) as applied to photothermal therapy (PTT). Starting from biogenic tabasheer extracted from bamboo and FeO, the resultant FeSi NPs with a much lower band gap exhibited excellent optical absorption with a photothermal conversion efficiency of 76.

EVA1A (Eva-1 Homolog A) Promotes Endothelial Apoptosis and Inflammatory Activation Under Disturbed Flow Via Regulation of Autophagy.

Background: Hemodynamic wall shear stress (WSS) exerted on the endothelium by flowing blood determines the spatial distribution of atherosclerotic lesions. Disturbed flow (DF) with a low WSS magnitude and reversing direction promotes atherosclerosis by regulating endothelial cell (EC) viability and function, whereas un-DF which is unidirectional and of high WSS magnitude is atheroprotective. Here, we study the role of EVA1A (eva-1 homolog A), a lysosome and endoplasmic reticulum-associated protein linked to autophagy and apoptosis, in WSS-regulated EC dysfunction.

JAG1-NOTCH4 mechanosensing drives atherosclerosis.

Endothelial cell (EC) sensing of disturbed blood flow triggers atherosclerosis, a disease of arteries that causes heart attack and stroke, through poorly defined mechanisms. The Notch pathway plays a central role in blood vessel growth and homeostasis, but its potential role in sensing of disturbed flow has not been previously studied. Here, we show using porcine and murine arteries and cultured human coronary artery EC that disturbed flow activates the JAG1-NOTCH4 signaling pathway.