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10.1161/ATVBAHA.112.255471 http://scihub22266oqcxt.onion/10.1161/ATVBAHA.112.255471 C4568119!4568119 !22814745     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=22814745 &cmd=llinks): Failed to open stream: HTTP request failed! 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Cholesterol-induced membrane microvesicles as novel carriers of damage-associated molecular patterns: mechanisms of formation, action, and detoxification |pdf=|usr=}}{{22814745 }} gab.com Text Cholesterol-induced membrane microvesicles as novel carriers of damage-associated molecular patterns: mechanisms of formation, action, and detoxification JO: Arterioscler Thromb Vasc Biol http://www.kidney.de/pget.php?&tw=1&pmid=22814745 #FOAvip OBJECTIVE: Cholesterol enrichment occurs in vivo when phagocytes ingest retained and aggregated lipoproteins, damaged or senescent cells, and related debris. We previously reported that enrichment of human monocyte/macrophages with unesterified cholesterol (UC) triggers the release of highly procoagulant microvesicles ([MVs], also called microparticles) through induction of apoptosis. We determined whether UC-induced MVs (UCMVs) might transmit endogenous danger signals and, if so, what molecular processes might be responsible for their production, recognition, and detoxification. METHODS AND RESULTS: Injection of UCMVs into rats provoked extensive leukocyte rolling and adherence to postcapillary venules in vivo. Likewise, exposure of mouse aortic explants or cultured human endothelial cells to UCMVs augmented the adhesion of human monocytes by several fold and increased endothelial cell intercellular adhesion molecule-1 via nuclear factor-?B activation. To explore molecular mechanisms, we found that UC enrichment of human monocytes, in the absence of other stimuli, induced mitochondrial complex II-dependent accumulation of superoxide and peroxides. A subset of these moieties was exported on UCMVs and mediated endothelial activation. Strikingly, aortic explants from mice lacking lectin-like oxidized low-density lipoprotein receptor-1, a pattern-recognition receptor, were essentially unable to respond to UCMVs, whereas simultaneously treated explants from wild-type mice responded robustly by increasing monocyte recruitment. Moreover, high-density lipoprotein and its associated enzyme paraoxonase-1 exerted unexpected roles in the detoxification of UCMVs. CONCLUSIONS: Overall, our study implicates MVs from cholesterol-loaded human cells as novel carriers of danger signals. By promoting maladaptive immunologic and thrombotic responses, these particles may contribute to atherothrombosis and other conditions in vivo. Twit Text FOAVip Cholesterol-induced membrane microvesicles as novel carriers of damage-associated molecular patterns: mechanisms of formation, action, and detoxification ????Arterioscler Thromb Vasc Biol http://www.kidney.de/pget.php?&tw=1&pmid=22814745 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22814745 #FOAvip English Wikipedia <ref>{{Cite pmid|22814745 }}</ref> Cholesterol-induced membrane microvesicles as novel carriers of damage-associated molecular patterns: mechanisms of formation, action, and detoxification #MMPMID22814745 Liu ML ; Scalia R ; Mehta JL ; Williams KJ Arterioscler Thromb Vasc Biol 2012[Sep]; 32 (9 ): 2113-21 PMID22814745 show ga OBJECTIVE: Cholesterol enrichment occurs in vivo when phagocytes ingest retained and aggregated lipoproteins, damaged or senescent cells, and related debris. We previously reported that enrichment of human monocyte/macrophages with unesterified cholesterol (UC) triggers the release of highly procoagulant microvesicles ([MVs], also called microparticles) through induction of apoptosis. We determined whether UC-induced MVs (UCMVs) might transmit endogenous danger signals and, if so, what molecular processes might be responsible for their production, recognition, and detoxification. METHODS AND RESULTS: Injection of UCMVs into rats provoked extensive leukocyte rolling and adherence to postcapillary venules in vivo. Likewise, exposure of mouse aortic explants or cultured human endothelial cells to UCMVs augmented the adhesion of human monocytes by several fold and increased endothelial cell intercellular adhesion molecule-1 via nuclear factor-?B activation. To explore molecular mechanisms, we found that UC enrichment of human monocytes, in the absence of other stimuli, induced mitochondrial complex II-dependent accumulation of superoxide and peroxides. A subset of these moieties was exported on UCMVs and mediated endothelial activation. Strikingly, aortic explants from mice lacking lectin-like oxidized low-density lipoprotein receptor-1, a pattern-recognition receptor, were essentially unable to respond to UCMVs, whereas simultaneously treated explants from wild-type mice responded robustly by increasing monocyte recruitment. Moreover, high-density lipoprotein and its associated enzyme paraoxonase-1 exerted unexpected roles in the detoxification of UCMVs. CONCLUSIONS: Overall, our study implicates MVs from cholesterol-loaded human cells as novel carriers of danger signals. By promoting maladaptive immunologic and thrombotic responses, these particles may contribute to atherothrombosis and other conditions in vivo. |*Signal Transduction [MESH] |Animals [MESH] |Aorta/metabolism [MESH] |Aryldialkylphosphatase/metabolism [MESH] |Cell Adhesion [MESH] |Cell Adhesion Molecules/metabolism [MESH] |Cell-Derived Microparticles/immunology/*metabolism [MESH] |Cells, Cultured [MESH] |Cholesterol/administration & dosage/*metabolism [MESH] |Coculture Techniques [MESH] |Electron Transport Complex II/metabolism [MESH] |Endothelial Cells/immunology/*metabolism [MESH] |Epitopes [MESH] |Human Umbilical Vein Endothelial Cells/metabolism [MESH] |Humans [MESH] |Hydrogen Peroxide/metabolism [MESH] |Injections, Intravenous [MESH] |Leukocyte Rolling [MESH] |Lipid Peroxidation [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Mitochondria/metabolism [MESH] |Monocytes/immunology/*metabolism [MESH] |NF-kappa B/metabolism [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH] |Scavenger Receptors, Class E/deficiency/genetics/metabolism [MESH] |Superoxides/metabolism [MESH] |Tissue Culture Techniques [MESH]Cholesterol-induced membrane microvesicles as novel carriers of damage(epmc).pdf DeepDyve Pubget Overpricing