2012
DOI: 10.1161/jaha.112.000992
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Abstract: BackgroundMacrophage‐mediated chronic inflammation is mechanistically linked to insulin resistance and atherosclerosis. Although arginase I is considered antiinflammatory, the role of arginase II (Arg‐II) in macrophage function remains elusive. This study characterizes the role of Arg‐II in macrophage inflammatory responses and its impact on obesity‐linked type II diabetes mellitus and atherosclerosis.Methods and ResultsIn human monocytes, silencing Arg‐II decreases the monocytes’ adhesion to endothelial cells… Show more

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Cited by 116 publications
(204 citation statements)
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“…Both pro (39)-and anti-inflammatory (40) consequences have been linked with Arg2 expression. A recent report used genetic approaches to demonstrate a proinflammatory role of Arg2 in the development of type 2 diabetes (T2D) and atherosclerosis (41). Our findings of higher Arg1 and blunted induction of Arg2 in the iPLA 2 ␤ Ϫ/Ϫ , relative to WT macrophages support the possibility that Arg2 is a proinflammatory marker under classical activation conditions, as might exist in an in vivo inflamma- iPLA 2 ␤ and Macrophage Polarization OCTOBER 28, 2016 • VOLUME 291 • NUMBER 44 tory milieu such as T1D.…”
Section: Discussionmentioning
confidence: 99%
“…Both pro (39)-and anti-inflammatory (40) consequences have been linked with Arg2 expression. A recent report used genetic approaches to demonstrate a proinflammatory role of Arg2 in the development of type 2 diabetes (T2D) and atherosclerosis (41). Our findings of higher Arg1 and blunted induction of Arg2 in the iPLA 2 ␤ Ϫ/Ϫ , relative to WT macrophages support the possibility that Arg2 is a proinflammatory marker under classical activation conditions, as might exist in an in vivo inflamma- iPLA 2 ␤ and Macrophage Polarization OCTOBER 28, 2016 • VOLUME 291 • NUMBER 44 tory milieu such as T1D.…”
Section: Discussionmentioning
confidence: 99%
“…Macrophages isolated from mice deficient in the autophagy proteins LC3B and ATG16L1 have enhanced NLRP3 inflammasome activation and produced higher IL-1b and IL-18 on LPS challenge (310,367). MtROS has also been implicated in increasing oxidative stress through cross-talk with nitric oxide synthases (NOSs) (293 the macrophage inflammatory response that contributes to insulin resistance and atherogenesis (293). Recent reports have highlighted an interesting concept of cross-talk between MtROS and NADPH oxidase, which can drive both feed-forward and feedback regulations of NADPH oxidases (73,96).…”
Section: B Mitochondrial-derived Ros In Inflammationmentioning
confidence: 99%
“…Compelling evidence implicates that Arg-II plays a dominant role in eNOSuncoupling in human and mouse blood vessels [10,11]. Our recent studies demonstrate that genetic ablation of Arg-II in mice reduces atherosclerosis on the ApoE -/-background, improves glucose homeostasis and insulin sensitivity in mice fed a high fat diet (HFD), which is at least partly attributable to dampening of macrophage inflammatory responses [12]. Moreover, genetic ablation of Arg-II slows down endothelial senescence and protects mice from age-associated endothelial inflammatory responses through inhibition of eNOS-uncoupling [10], implying a causative role of Arg-II in eNOS-uncoupling and endothelial dysfunction in aging.…”
Section: Introductionmentioning
confidence: 93%
“…Preparation of mouse aortic tissue and endothelium cell extract, SDS-PAGE, transfer of SDS gels to an Immobilon-P membrane (Millipore) were performed as previously described [12]. The resultant membrane was incubated overnight with the corresponding primary antibody (1:2500 for eNOS, 1:500 for phosphoSer1177-eNOS, 1:200 for arginase-II and 1:1000 for p38mapk and phospho-Thr180/Tyr182-p38mapk) at 4°C with gentle agitation after blocking with 5% skimmed milk.…”
Section: Immunoblotting Analysismentioning
confidence: 99%