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10.1016/j.bbalip.2014.02.006 http://scihub22266oqcxt.onion/10.1016/j.bbalip.2014.02.006 C3996726!3996726!24603323     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Biochim+Biophys+Acta 2014 ; 1841 (6): 827-35 Nephropedia Template TP {{tp|p=24603323|t=2014. miR-206 controls LXR? expression and promotes LXR-mediated cholesterol efflux in macrophages |pdf=|usr=}}{{24603323}} gab.com Text miR-206 controls LXR expression and promotes LXR-mediated cholesterol efflux in macrophages JO: Biochim Biophys Acta http://www.kidney.de/pget.php?&tw=1&pmid=24603323 #FOAvip Liver X receptors (LXR? and LXR?) are key transcription factors in cholesterol metabolism that regulate cholesterol biosynthesis/efflux and bile acid metabolism/excretion in the liver and numerous organs. In macrophages, LXR signaling modulates cholesterol handling and the inflammatory response, pathways involved in atherosclerosis. Since regulatory pathways of LXR transcription control are well understood, in the present study we aimed at identifying post-transcriptional regulators of LXR activity. MicroRNAs (miRs) are such post-transcriptional regulators of genes that in the canonical pathway mediate mRNA inactivation. In silico analysis identified miR-206 as a putative regulator of LXR? but not LXR?. Indeed, as recently shown, we found that miR-206 represses LXR? activity and expression of LXR? and its target genes in hepatic cells. Interestingly, miR-206 regulates LXR? differently in macrophages. Stably overexpressing miR-206 in THP-1 human macrophages revealed an up-regulation and miR-206 knockdown led to a down-regulation of LXR? and its target genes. In support of these results, bone marrow-derived macrophages (BMDMs) from miR-206 KO mice also exhibited lower expression of LXR? target genes. The physiological relevance of these findings was proven by gain- and loss-of-function of miR-206; overexpression of miR-206 enhanced cholesterol efflux in human macrophages and knocking out miR-206 decreased cholesterol efflux from MPMs. Moreover, we show that miR-206 expression in macrophages is repressed by LXR? activation, while oxidized LDL and inflammatory stimuli profoundly induced miR-206 expression. We therefore propose a feed-back loop between miR-206 and LXR? that might be part of an LXR auto-regulatory mechanism to fine tune LXR activity. Twit Text FOAVip miR-206 controls LXR expression and promotes LXR-mediated cholesterol efflux in macrophages ????Biochim Biophys Acta http://www.kidney.de/pget.php?&tw=1&pmid=24603323 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24603323 #FOAvip English Wikipedia <ref>{{Cite pmid|24603323}}</ref> miR-206 controls LXR? expression and promotes LXR-mediated cholesterol efflux in macrophages #MMPMID24603323 Vinod M; Chennamsetty I; Colin S; Belloy L; De Paoli F; Schaider H; Graier WF; Frank S; Kratky D; Staels B; Chinetti-Gbaguidi G; Kostner GM Biochim Biophys Acta 2014[Jun]; 1841 (6): 827-35 PMID24603323show ga Liver X receptors (LXR? and LXR?) are key transcription factors in cholesterol metabolism that regulate cholesterol biosynthesis/efflux and bile acid metabolism/excretion in the liver and numerous organs. In macrophages, LXR signaling modulates cholesterol handling and the inflammatory response, pathways involved in atherosclerosis. Since regulatory pathways of LXR transcription control are well understood, in the present study we aimed at identifying post-transcriptional regulators of LXR activity. MicroRNAs (miRs) are such post-transcriptional regulators of genes that in the canonical pathway mediate mRNA inactivation. In silico analysis identified miR-206 as a putative regulator of LXR? but not LXR?. Indeed, as recently shown, we found that miR-206 represses LXR? activity and expression of LXR? and its target genes in hepatic cells. Interestingly, miR-206 regulates LXR? differently in macrophages. Stably overexpressing miR-206 in THP-1 human macrophages revealed an up-regulation and miR-206 knockdown led to a down-regulation of LXR? and its target genes. In support of these results, bone marrow-derived macrophages (BMDMs) from miR-206 KO mice also exhibited lower expression of LXR? target genes. The physiological relevance of these findings was proven by gain- and loss-of-function of miR-206; overexpression of miR-206 enhanced cholesterol efflux in human macrophages and knocking out miR-206 decreased cholesterol efflux from MPMs. Moreover, we show that miR-206 expression in macrophages is repressed by LXR? activation, while oxidized LDL and inflammatory stimuli profoundly induced miR-206 expression. We therefore propose a feed-back loop between miR-206 and LXR? that might be part of an LXR auto-regulatory mechanism to fine tune LXR activity. ämiR-206 controls LXR? expression and promotes LXR-mediated cholesterol(epmc).pdf DeepDyve Pubget Overpricing