Publications by authors named "W C Sessa"
The dorsal aorta (DA) is the first major blood vessel to develop in the embryonic cardiovascular system. Its formation is governed by a coordinated process involving the migration, specification, and arrangement of angioblasts into arterial and venous lineages, a process conserved across species. Although vascular endothelial growth factor a (VEGF-A) is known to drive DA specification and formation, the kinases involved in this process remain ambiguous.
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- - ZFYVE21 is a protein found in endothelial cells that plays a key role in maintaining vascular barrier function, especially in aging kidneys, but its exact functions were previously unclear.
- - In a study, researchers created mice that lack ZFYVE21 specifically in endothelial cells, revealing that these mice exhibited serious health issues such as reduced nitric oxide activity and kidney problems as they aged.
- - The study indicates that ZFYVE21 influences the movement of certain proteins within cells to keep endothelial nitric oxide synthase (ENOS) active, which is important for kidney function in older individuals.
Blood vessels are continually exposed to circulating lipids, and elevation of ApoB-containing lipoproteins causes atherosclerosis. Lipoprotein metabolism is highly regulated by lipolysis, largely at the level of the capillary endothelium lining metabolically active tissues. How large blood vessels, the site of atherosclerotic vascular disease, regulate the flux of fatty acids (FAs) into triglyceride-rich (TG-rich) lipid droplets (LDs) is not known.
View Article and Find Full Text PDFObjective: We have previously demonstrated the importance of the Akt-eNOS substrate-kinase relationship, as defective postnatal angiogenesis characteristic of global Akt1-null mice is rescued when bred to 'gain-of-function' eNOS S1176D mutant mice. While multiple studies support the vascular protective role of endothelial NO generation, the causal role of Akt1-dependent eNOS S1176 phosphorylation during atherosclerotic plaque formation is not yet clear.
Approach And Results: We herein bred congenic 'loss-of-function' eNOS S1176A and 'gain-of-function' eNOS S1176D mutant mice to the exacerbated atherogenic Akt1; ApoE double knockout mice to definitively test the importance of Akt-mediated eNOS S1176 phosphorylation during atherogenesis.