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10.1172/JCI75005 http://scihub22266oqcxt.onion/10.1172/JCI75005 C5531402!5531402 !28650342     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28650342 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Clin+Invest 2017 ; 127 (8 ): 2904-2915 Nephropedia Template TP {{tp|p=28650342 |t=2017. Inflammatory Ly6Chi monocytes and their conversion to M2 macrophages drive atherosclerosis regression |pdf=|usr=}}{{28650342 }} gab.com Text Inflammatory Ly6Chi monocytes and their conversion to M2 macrophages drive atherosclerosis regression JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=28650342 #FOAvip Atherosclerosis is a chronic inflammatory disease, and developing therapies to promote its regression is an important clinical goal. We previously established that atherosclerosis regression is characterized by an overall decrease in plaque macrophages and enrichment in markers of alternatively activated M2 macrophages. We have now investigated the origin and functional requirement for M2 macrophages in regression in normolipidemic mice that received transplants of atherosclerotic aortic segments. We compared plaque regression in WT normolipidemic recipients and those deficient in chemokine receptors necessary to recruit inflammatory Ly6Chi (Ccr2-/- or Cx3cr1-/-) or patrolling Ly6Clo (Ccr5-/-) monocytes. Atherosclerotic plaques transplanted into WT or Ccr5-/- recipients showed reduced macrophage content and increased M2 markers consistent with plaque regression, whereas plaques transplanted into Ccr2-/- or Cx3cr1-/- recipients lacked this regression signature. The requirement of recipient Ly6Chi monocyte recruitment was confirmed in cell trafficking studies. Fate-mapping and single-cell RNA sequencing studies also showed that M2-like macrophages were derived from newly recruited monocytes. Furthermore, we used recipient mice deficient in STAT6 to demonstrate a requirement for this critical component of M2 polarization in atherosclerosis regression. Collectively, these results suggest that continued recruitment of Ly6Chi inflammatory monocytes and their STAT6-dependent polarization to the M2 state are required for resolution of atherosclerotic inflammation and plaque regression. Twit Text FOAVip Inflammatory Ly6Chi monocytes and their conversion to M2 macrophages drive atherosclerosis regression ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=28650342 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28650342 #FOAvip English Wikipedia <ref>{{Cite pmid|28650342 }}</ref> Inflammatory Ly6Chi monocytes and their conversion to M2 macrophages drive atherosclerosis regression #MMPMID28650342 Rahman K ; Vengrenyuk Y ; Ramsey SA ; Vila NR ; Girgis NM ; Liu J ; Gusarova V ; Gromada J ; Weinstock A ; Moore KJ ; Loke P ; Fisher EA J Clin Invest 2017[Aug]; 127 (8 ): 2904-2915 PMID28650342 show ga Atherosclerosis is a chronic inflammatory disease, and developing therapies to promote its regression is an important clinical goal. We previously established that atherosclerosis regression is characterized by an overall decrease in plaque macrophages and enrichment in markers of alternatively activated M2 macrophages. We have now investigated the origin and functional requirement for M2 macrophages in regression in normolipidemic mice that received transplants of atherosclerotic aortic segments. We compared plaque regression in WT normolipidemic recipients and those deficient in chemokine receptors necessary to recruit inflammatory Ly6Chi (Ccr2-/- or Cx3cr1-/-) or patrolling Ly6Clo (Ccr5-/-) monocytes. Atherosclerotic plaques transplanted into WT or Ccr5-/- recipients showed reduced macrophage content and increased M2 markers consistent with plaque regression, whereas plaques transplanted into Ccr2-/- or Cx3cr1-/- recipients lacked this regression signature. The requirement of recipient Ly6Chi monocyte recruitment was confirmed in cell trafficking studies. Fate-mapping and single-cell RNA sequencing studies also showed that M2-like macrophages were derived from newly recruited monocytes. Furthermore, we used recipient mice deficient in STAT6 to demonstrate a requirement for this critical component of M2 polarization in atherosclerosis regression. Collectively, these results suggest that continued recruitment of Ly6Chi inflammatory monocytes and their STAT6-dependent polarization to the M2 state are required for resolution of atherosclerotic inflammation and plaque regression. |Animals [MESH] |Aorta/metabolism/physiology [MESH] |Atherosclerosis/*blood/metabolism [MESH] |CX3C Chemokine Receptor 1 [MESH] |Cell Lineage [MESH] |Female [MESH] |Hyperlipidemias/blood [MESH] |Inflammation [MESH] |Macrophages/*cytology/metabolism [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Monocytes/*cytology/metabolism [MESH] |Phenotype [MESH] |Plaque, Atherosclerotic/*blood/metabolism [MESH] |Receptors, CCR2/genetics [MESH] |Receptors, CCR5/genetics [MESH] |Receptors, Chemokine/genetics [MESH] |STAT6 Transcription Factor/metabolism [MESH] |Sequence Analysis, RNA [MESH]Inflammatory Ly6Chi monocytes and their conversion to M2 macrophages d(epmc).pdf DeepDyve Pubget Overpricing