High glucose downregulates the number of caveolae in monocytes through oxidative stress from NADPH oxidase: Implications for atherosclerosis

Hayashi, Toshio; Juliet, Packiasamy A.R.; Miyazaki, Asaka; Ignarro, Louis J.; Iguchi, Akihisa

doi:10.1016/j.bbadis.2006.11.011

Cited by 49 publications

(46 citation statements)

References 43 publications

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“…The deacylation/reacylation reaction of eNOS in the plasmalemmal caveolae regulates NO production (Napoli et al, 2006;Lim et al, 2007;Hayashi et al, 2007). Acylation targets the localization of eNOS to plasmalemmal caveolae, a site where the enzyme activity is inhibited through association with caveolin.…”

Section: Molecular Mechanisms Regula-ting Enosmentioning

confidence: 99%

Nitric oxide and pathogenic mechanisms involved in the development of vascular diseases

2009

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Nitric oxide (NO) is a pivotal signaling messenger in the cardiovascular system. NO participates in regulatory functions including control of hemostasis, fibrinolysis, platelet and leukocyte interactions with the arterial wall, regulation of vascular tone, proliferation of vascular smooth muscle cells, and homeostasis of blood pressure. Diminished NO bioavailability and abnormalities in NO-dependent signaling are among central factors of vascular disease, although it is unclear whether this is a cause of, or result of endothelial dysfunction or both pathogenic events. Disturbances in NO bioavailability have been linked to cause endothelial dysfunction, leading to increased susceptibility to atherosclerotic lesion progression, hypertension, hypercholesterolemia, diabetes mellitus, thrombosis and stroke.

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Section: Molecular Mechanisms Regula-ting Enosmentioning

confidence: 99%

Nitric oxide and pathogenic mechanisms involved in the development of vascular diseases

2009

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“…It is likely therefore that activation of these pathways acts in concert with many of the other mechanisms mentioned above. There are numerous potential causes of ER stress that have been implicated in atheropathogenesis, examples of which include: oxysterol [105], NO [113], ubiquitin-proteasome system (UPS) [114], insulin resistance [115], unfolded protein response (UPR) [116], forkhead transcription factor (FoxO)1 [117], calcium [118], 7-ketocholesterol [119], NADPH oxidase [120]. Insulin resistance is a well documented risk factor for atherosclerosis, however the exact mechanism remains unknown.…”

Section: Macrovascular Complications-cardiovascular Disease and Macromentioning

confidence: 99%

Diabetes mellitus and apoptosis: inflammatory cells

et al. 2009

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Since the early observation that similarities between thyroiditis and insulitis existed, the important role played by inflammation in the development of diabetes has been appreciated. More recently, experiments have shown that inflammation also plays a prominent role in the development of target organ damage arising as complications, with both elements of the innate and the adaptive immune system being involved, and that cytokines contributing to local tissue damage may arise from both infiltrating and resident cells. This review will discuss the experimental evidence that shows that inflammatory cellmediated apoptosis contributes to target organ damage, from beta cell destruction to both micro-and macro-vascular disease complications, and also how alterations in leukocyte turnover affects immune function.

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“…We evaluated the relationship between the expression of Cav-1 and the number of caveolae in macrophages under conditions of high glucose concentration. 57 Increased superoxide production, induction of iNOS and decreased Cav-1 were observed in a concentration-dependent manner in THP-1-derived macrophages with high glucose. Co-localization of the NADPH oxidase component, p47phox, and caveolin was confirmed by confocal microscopy.…”

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confidence: 92%

“…Caveolin-1 (Cav-1) has a critical role in the development of atherosclerosis. 57 Cav-1 is associated with cholesteryl ester uptake from LDL (but not oxidized LDL) and with cholesterol reverse transport by high-density lipoprotein in THP-1 macrophages. Insulin signaling for metabolic control depends on intact caveolae, and destruction of caveolae disrupts insulin-stimulated phosphorylation of insulin receptor substrate-1.…”

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confidence: 98%

Possibility of the regression of atherosclerosis through the prevention of endothelial senescence by the regulation of nitric oxide and free radical scavengers

Hayashi

Iguchi

2010

Geriatrics Gerontology Int

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In the elderly, atherosclerotic diseases such as stroke and myocardial infarction occupy a major part of their causes of death and care. The elderly always have atherosclerosis in their aorta and other arteries and are exposed to risk of attacks. It is the elderly who should receive its safe, harmless and advanced treatment. Advanced stage of atherosclerosis in the elderly is progressed by complicated risk factors such as dyslipidemia and diabetes mellitus and specific risk factors for the elderly, aging (and menopause). Treatment of atherosclerotic disease may need special ones targeted for the elderly. Recent studies reported that frequencies of dyslipidemia were not decreased in the older oldest. In the elderly, impaired glucose tolerance occurrs and it progresses atherosclerosis. Endothelial dysfunction like impairment of nitric oxide (NO) bioavailability also progresses atherosclerosis. Although we tried to regress the high cholesterol diet-induced atherosclerosis in rabbit aorta with a normal diet with or without statin, regression could not be achieved. NO targeting gene therapy (adenovirus endothelial nitric oxide synthase [eNOS] gene vector) regressed 20% of atherosclerotic lesions through reduction of lipid contents, however, a more integrated strategy is important for complete regression. We paid attention to NO bioavailability and developed two ways of increasing it in atherosclerosis: citrulline therapy and arginase II inhibition by estrogen. Further, we found a close relation between atherosclerosis and endothelial senescence and that NO can prevent it, especially in a diabetic model. Taken together, regression of atherosclerosis can be achieved by not only regulation of various risk factors but regulation of the cross-talk of NO and free radicals. Geriatr Gerontol Int 2010; 10: 115-130.

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High glucose downregulates the number of caveolae in monocytes through oxidative stress from NADPH oxidase: Implications for atherosclerosis

Cited by 49 publications

References 43 publications

Nitric oxide and pathogenic mechanisms involved in the development of vascular diseases

Nitric oxide and pathogenic mechanisms involved in the development of vascular diseases

Diabetes mellitus and apoptosis: inflammatory cells

Possibility of the regression of atherosclerosis through the prevention of endothelial senescence by the regulation of nitric oxide and free radical scavengers

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