2009
DOI: 10.1186/1471-2261-9-12
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Abstract: Background: Pharmacological inhibition of endothelial arginase-II has been shown to improve endothelial nitric oxide synthase (eNOS) function and reduce atherogenesis in animal models. We investigated whether the endothelial arginase II is involved in inflammatory responses in endothelial cells.

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Cited by 58 publications
(38 citation statements)
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“…Generation of rAd expressing shRNA targeting human Arg-II and S6K1 driven by the U6 promoter (rAd/U6-hArg-II shRNA and -hS6K1 shRNA , respectively) was described previously [48] The control rAd expressing shRNA targeting LacZ (rAd/U6-LacZ shRNA ) was from Invitrogen life Technologies. The rAd titer (infectious unit: ifu/ml) was determined by staining the largest and most abundant structural proteins “hexon proteins” in the adenovirus capsid using QuickTiter™ Adenovirus Titer Immunoassay Kit after infecting HER911 cells, derived from human retina cells by Adenovirus E1 transformation [49], for 48 hours.…”
Section: Methodsmentioning
confidence: 99%
“…Generation of rAd expressing shRNA targeting human Arg-II and S6K1 driven by the U6 promoter (rAd/U6-hArg-II shRNA and -hS6K1 shRNA , respectively) was described previously [48] The control rAd expressing shRNA targeting LacZ (rAd/U6-LacZ shRNA ) was from Invitrogen life Technologies. The rAd titer (infectious unit: ifu/ml) was determined by staining the largest and most abundant structural proteins “hexon proteins” in the adenovirus capsid using QuickTiter™ Adenovirus Titer Immunoassay Kit after infecting HER911 cells, derived from human retina cells by Adenovirus E1 transformation [49], for 48 hours.…”
Section: Methodsmentioning
confidence: 99%
“…Because of the complex interaction among these events, it is not easy to delineate their causal relationship in the pathogenesis of vascular diseases. Under physiological conditions, in the absence of risk factors, the endothelial cells express negligible levels of adhesion molecules such as ICAM-1 and VCAM-1 for inflammatory cells and low levels of the coagulation enzyme tissue factor (Viswambharan et al, 2004; Ming et al, 2009, 2010), whereas in the presence of the risk factors, these molecules are up-regulated in the cells, which may enhance monocyte–endothelial cell interaction and activation of coagulation cascade, participating in the initiation and progression of atherosclerotic plaque formation and thrombus formation (Camici et al, 2006). The role of inflammation and underlying mechanisms in atherogenesis and atherothrombosis are comprehensively reviewed by many articles (Faxon et al, 2004; Hansson and Hermansson, 2011; Lonn et al, 2012).…”
Section: Oxidative Stress Inflammation and Vascular Diseasementioning
confidence: 99%
“…To examine how the L57A mutation improves the catalytic potential of OATA for the production of bulky unnatural amino acids, we carried out the asymmetric synthesis of L-norvaline, which is a key intermediate of perindopril (i.e., an angiotensinconverting enzyme inhibitor) (41) and a potential inhibitor of arginase (42). As expected, the L57A variant afforded a much faster synthesis of L-norvaline from 50 mM 2-oxopentanoic acid and 100 mM isopropylamine than its parental enzyme did under the same reaction conditions (Fig.…”
mentioning
confidence: 99%