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10.1038/cr.2017.8 http://scihub22266oqcxt.onion/10.1038/cr.2017.8 C5339843!5339843!28084332     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Res 2017 ; 27 (3): 352-72 Nephropedia Template TP {{tp|p=28084332|t=2017. Macrophagic CD146 promotes foam cell formation and retention during atherosclerosis |pdf=|usr=}}{{28084332}} gab.com Text Macrophagic CD146 promotes foam cell formation and retention during atherosclerosis JO: Cell Res http://www.kidney.de/pget.php?&tw=1&pmid=28084332 #FOAvip The persistence of cholesterol-engorged macrophages (foam cells) in the artery wall fuels the development of atherosclerosis. However, the mechanism that regulates the formation of macrophage foam cells and impedes their emigration out of inflamed plaques is still elusive. Here, we report that adhesion receptor CD146 controls the formation of macrophage foam cells and their retention within the plaque during atherosclerosis exacerbation. CD146 is expressed on the macrophages in human and mouse atheroma and can be upregulated by oxidized low-density lipoprotein (oxLDL). CD146 triggers macrophage activation by driving the internalization of scavenger receptor CD36 during lipid uptake. In response to oxLDL, macrophages show reduced migratory capacity toward chemokines CCL19 and CCL21; this capacity can be restored by blocking CD146. Genetic deletion of macrophagic CD146 or targeting of CD146 with an antibody result in much less complex plaques in high-fat diet-fed ApoE?/? mice by causing lipid-loaded macrophages to leave plaques. Collectively, our findings identify CD146 as a novel retention signal that traps macrophages within the artery wall, and a promising therapeutic target in atherosclerosis treatment. Twit Text FOAVip Macrophagic CD146 promotes foam cell formation and retention during atherosclerosis ????Cell Res http://www.kidney.de/pget.php?&tw=1&pmid=28084332 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28084332 #FOAvip English Wikipedia <ref>{{Cite pmid|28084332}}</ref> Macrophagic CD146 promotes foam cell formation and retention during atherosclerosis #MMPMID28084332 Luo Y; Duan H; Qian Y; Feng L; Wu Z; Wang F; Feng J; Yang D; Qin Z; Yan X Cell Res 2017[Mar]; 27 (3): 352-72 PMID28084332show ga The persistence of cholesterol-engorged macrophages (foam cells) in the artery wall fuels the development of atherosclerosis. However, the mechanism that regulates the formation of macrophage foam cells and impedes their emigration out of inflamed plaques is still elusive. Here, we report that adhesion receptor CD146 controls the formation of macrophage foam cells and their retention within the plaque during atherosclerosis exacerbation. CD146 is expressed on the macrophages in human and mouse atheroma and can be upregulated by oxidized low-density lipoprotein (oxLDL). CD146 triggers macrophage activation by driving the internalization of scavenger receptor CD36 during lipid uptake. In response to oxLDL, macrophages show reduced migratory capacity toward chemokines CCL19 and CCL21; this capacity can be restored by blocking CD146. Genetic deletion of macrophagic CD146 or targeting of CD146 with an antibody result in much less complex plaques in high-fat diet-fed ApoE?/? mice by causing lipid-loaded macrophages to leave plaques. Collectively, our findings identify CD146 as a novel retention signal that traps macrophages within the artery wall, and a promising therapeutic target in atherosclerosis treatment. äMacrophagic CD146 promotes foam cell formation and retention during at(epmc).pdf DeepDyve Pubget Overpricing