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Corneal avascularity is due to soluble VEGF receptor-1
TLDR
It is shown that the cornea expresses soluble VEGF receptor-1 (sVEGFR-1; also known as sflt-1) and that suppression of this endogenous V EGF-A trap by neutralizing antibodies, RNA interference or Cre-lox-mediated gene disruption abolishes corneal avascularity in mice. Expand
Vascular Endothelial Growth Factor Signals Endothelial Cell Production of Nitric Oxide and Prostacyclin through Flk-1/KDR Activation of c-Src*
TLDR
The results suggest that NO and PGI2 function in parallel in mediating the effects of VEGF, and that Src activation is required for V EGF induction of phospholipase C γ1 activation and inositol 1,4,5-trisphosphate formation. Expand
Diabetes-induced Coronary Vascular Dysfunction Involves Increased Arginase Activity
TLDR
It is indicated that increased arginase activity in diabetes contributes to vascular endothelial dysfunction by decreasing l-arginine availability to NO synthase. Expand
Vascular endothelial growth factor and diabetic retinopathy: pathophysiological mechanisms and treatment perspectives
TLDR
The cellular and molecular alterations that characterize experimental models of diabetes are considered in relation to the influence of high glucose‐mediated oxidative stress on VEGF expression and on the mechanisms of V EGF's actions under hyperglycemic induction. Expand
Therapeutic use of citrulline in cardiovascular disease.
TLDR
Substantial intestinal and hepatic metabolism of L-arginine to ornithine and urea by arginase makes oral delivery very ineffective, and supplemental L-citrulline has promise as a therapeutic adjunct in disease states associated with L- arginine deficiencies. Expand
Neuroprotective and blood-retinal barrier-preserving effects of cannabidiol in experimental diabetes.
TLDR
It is demonstrated that CBD treatment reduces neurotoxicity, inflammation, and BRB breakdown in diabetic animals through activities that may involve inhibition of p38 MAP kinase. Expand
Experimental diabetes causes breakdown of the blood-retina barrier by a mechanism involving tyrosine nitration and increases in expression of vascular endothelial growth factor and urokinase
TLDR
Data indicate that early diabetes causes breakdown of the BRB by a mechanism involving the action of reactive nitrogen species in promoting expression of VEGF and uPAR. Expand
Prevention of diabetes-induced arginase activation and vascular dysfunction by Rho kinase (ROCK) knockout.
TLDR
Partial deletion of either ROCK isoform, but to a greater extent ROCK1, attenuates diabetes-induced vascular endothelial dysfunction by preventing increased arginase activity and expression and reduction in NO production in type 1 diabetes. Expand
Pravastatin sodium activates endothelial nitric oxide synthase independent of its cholesterol-lowering actions.
TLDR
Clinical benefits with PRA not explained by LDL reductions may be the result of an independent action of PRA on eNOS activation, but SIM is much less effective. Expand
VEGF induces nuclear translocation of Flk-1/KDR, endothelial nitric oxide synthase, and caveolin-1 in vascular endothelial cells.
TLDR
Nuclear translocation of eNOS and Flk-1/KDR within caveolae may represent a mechanism for targeting NO production to the nuclear compartment where it could influence transcription factor activation. Expand
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