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Dynamic activation of endothelial nitric oxide synthase by Hsp90
TLDR
Inhibition of signalling through Hsp90 attenuates both agonist-stimulated production of nitric oxide and endothelium-dependent relaxation of isolated blood vessels and indicates that in addition to its role as a molecular chaperone involved in protein folding and maturation, HSp90 may also be recruited to cellular targets depending on the activation state of the cell. Expand
Biological action of leptin as an angiogenic factor.
TLDR
It is shown that OB-Rb is also expressed in human vasculature and in primary cultures of human endothelial cells, indicating that the vascular endothelium is a target for leptin and suggesting a physiological mechanism whereby leptin-induced angiogenesis may facilitate increased energy expenditure. Expand
Integration of flow-dependent endothelial phenotypes by Kruppel-like factor 2.
TLDR
KLF2 therefore serves as a mechano-activated transcription factor important in the integration of multiple endothelial functions associated with regions of the arterial vasculature that are relatively resistant to atherogenesis. Expand
KLF2 Is a Novel Transcriptional Regulator of Endothelial Proinflammatory Activation
TLDR
The studies implicate recruitment by KLF2 of the transcriptional coactivator cyclic AMP response element–binding protein (CBP/p300) as a unifying mechanism for these various effects of proinflammatory stimuli. Expand
Nitric oxide production contributes to the angiogenic properties of vascular endothelial growth factor in human endothelial cells.
TLDR
Both short- and long-term exposure of human EC to VEGF stimulates the release of biologically active NO, suggesting that NO mediates aspects of V EGF signaling required for EC proliferation and organization in vitro. Expand
Dissecting the Interaction between Nitric Oxide Synthase (NOS) and Caveolin
TLDR
The data demonstrate a novel functional role for Caveolin-1 in mammalian cells as a potential molecular chaperone that directly inactivates NOS and the inactivation of eNOS and nNOS by the scaffolding domain of caveolin-3 suggests that eN OS in cardiac myocytes and n NOS in skeletal muscle are likely subject to negative regulation by this muscle-specific caveolin isoform. Expand
Distinct endothelial phenotypes evoked by arterial waveforms derived from atherosclerosis-susceptible and -resistant regions of human vasculature.
TLDR
An in vitro dynamic flow system is used to accurately reproduce arterial shear stress waveforms on cultured human EC and global gene expression patterns and functional data reveal a distinct phenotypic modulation in response to the wall shear stresses present in atherosclerosis-susceptible vs. atheros sclerosis-resistant human arterial geometries. Expand
Recent insights into the cellular biology of atherosclerosis
TLDR
Recent advances in atherosclerosis highlight important cell biological atherogenic processes, including mechanotransduction and inflammatory processes in endothelial cells, origins and contributions of lesional macrophages, and origins and phenotypic switching ofLesional smooth muscle cells. Expand
Biomechanical forces promote embryonic haematopoiesis
TLDR
A critical role for biomechanical forces in haematopoietic development is revealed in mouse embryos using mouse embryonic stem cells differentiated in vitro and that abrogation of nitric oxide, a mediator of shear-stress-induced signalling, compromises haem atopOietic potential in vivo and in vivo is revealed. Expand
Endothelial Dysfunction, Hemodynamic Forces, and Atherogenesis a
TLDR
It is hypothesized that the selective and sustained expression of certain transcription factors and related “atheroprotective genes” in the endothelial lining of lesion‐protected areas represents a mechanism whereby hemodynamic forces can influence lesion formation and progression. Expand
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