Abstract:
:Microparticles are membrane vesicles with procoagulant and proinflammatory properties released during cell activation or apoptosis. Microparticles from monocytes have been implicated in atherosclerosis and vascular inflammation, but their direct effects on endothelial cells are not completely elucidated. The present study was designed to dissect the signaling pathways of monocytic microparticles in endothelial cells with respect to both NO pathway and reactive oxygen species. Microparticles were produced by treatment of human monocytic cell line THP-1 with the apoptotic agent VP-16. Human endothelial cells were treated with monocytic microparticles and then, we studied their effects on nitrosative and oxidative stresses. Incubation of human endothelial cells with microparticles enhanced the production of NO without affecting superoxide anions generation. Microparticles did not affect endothelial NO synthase expression and its phosphorylation. Interestingly, microparticles decreased caveolin-1 expression and increased its phosphorylation. Inhibition of PI-3-kinase or MEK1/2 reversed the effects of microparticles on caveolin-1 expression but not its phosphorylation. Moreover, microparticles increased nitration of several proteins, reflecting peroxynitrite production, which was prevented by blockade of PI-3-kinase pathway. In summary, monocyte microparticles active multiple pathways related to nitrosative stress in endothelial cells including both PI-3-kinase and ERK1/2 in the regulation of caveolin-1 expression. These data underscore the pleiotropic effect of microparticles on endothelial cells and suggest that they probably play a critical role on vascular function.
journal_name
Fundam Clin Pharmacoljournal_title
Fundamental & clinical pharmacologyauthors
Mastronardi ML,Mostefai HA,Soleti R,Agouni A,Martínez MC,Andriantsitohaina Rdoi
10.1111/j.1472-8206.2010.00898.xsubject
Has Abstractpub_date
2011-12-01 00:00:00pages
653-60issue
6eissn
0767-3981issn
1472-8206journal_volume
25pub_type
杂志文章abstract::Prostaglandin E synthase (PGES) is a recently identified terminal enzyme that acts downstream of cyclooxygenase and catalyzes the conversion of prostaglandin (PG) H2 to PGE2. At least three isozymes have been cloned so far, which are called membrane-associated PGES (mPGES)-1, mPGES-2, and cytosolic PGES. Among them, m...
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journal_title:Fundamental & clinical pharmacology
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journal_title:Fundamental & clinical pharmacology
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journal_title:Fundamental & clinical pharmacology
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doi:10.1111/j.1472-8206.2006.00441.x
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journal_title:Fundamental & clinical pharmacology
pub_type: 杂志文章
doi:10.1111/j.1472-8206.1994.tb00834.x
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journal_title:Fundamental & clinical pharmacology
pub_type: 杂志文章,评审
doi:10.1111/j.1472-8206.1995.tb00505.x
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doi:10.1111/j.1472-8206.2006.00458.x
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journal_title:Fundamental & clinical pharmacology
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abstract::This study evaluated the effect of lacosamide (LCM) on biochemical and mitochondrial parameters after PTZ kindling in mice. Male mice were treated on alternative days for a period of 11 days with LCM (20, 30, or 40 mg/kg), saline, or diazepam (2 mg/kg), before PTZ administration (50 mg/kg). The hippocampi were collect...
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abstract::The phylogenetically old renin-angiotensin-system (RAS) was originally described as a circulating hormonal system and a main cardiovascular regulator. However, there also exist 'local RASs' which are situated in cardiovascular as well as non-cardiovascular tissues where they are involved in physiological and patho-phy...
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