Synthetic agonists of liver X-receptors (LXR\u03b1, NR1H3 and LXR\u03b2, NR1H2) or cholesterol-loading signi\ufb01cantly induced the expression of ABCA1 protein in mouse RAW 264.7 and human THP-1 macrophage cell lines (Beyea MM et al. 2007; Ku CS et al. 2012). Similar regulation of ABCA1 protein expression by NR1H2, 3 agonists was observed in human peripheral blood-derived monocytes (Mauerer R et al. 2009). Treatment of THP-1 macrophages with endogenous (25-hydroxycholesterol) or synthetic (T0901317) ligands of NR1H2,3 stimulated both transcriptional and posttranscriptional pathways to enhance ABCA1 expression (Ignatova ID et al. 2013). Further, partial inhibition of oxidosqualene:lanosterol cyclase (OSC) stimulated synthesis of the NR1H2,3 agonist 24(S),25-epoxycholesterol (24(S),25-epoxy) and enhanced ABCA1-mediated cholesterol efflux in THP-1 cells (Beyea MM et al. 2007). NR1H3 and NR1H2-induced expression of ABCA1 is thought to promote cellular cholesterol transfer to lipid-poor apolipoproteins such as ApoA1 and ApoE in the formation of nascent HDL particles (Ignatova ID et al. 2013; Vedhachalam C et al. 2007). Loss of ABCA1 in humans results in Tangier disease, a condition in which patients have extremely low levels of circulating HDL, massive accumulation of cholesterol in macrophages, and an increased risk for developing atherosclerosis (Rust S et al. 1999).
MicroRNAs miR-26 and miR-33 negatively regulate the translation of ABCA1 mRNA and thus repress the NR1H2, NR1H3-dependent cholesterol efflux from macrophages (Sun D et al. 2012; Rayner KJ et al. 2010). MicroRNA miR-144 also binds the ABCA1 3\u2019UTR to prohibit translation and reduce ABCA1-mediated cholesterol efflux from hepatocytes (de Aguiar Vallim TQ et al. 2013)", "cellular_location": "cytosol, plasma membrane", "input_participant_list": [ "R-HSA-9618483" ], "output_participant_list": [], "enzyme_list": [ "O95477-1", "Q9UKV8-1", "Q9H9G7-1", "Q9HCE1-1" ], "evidence": [ { "id": "R-HSA-9618479", "database": "Reactome", "url": "https://www.reactome.org/PathwayBrowser/#R-HSA-9618479" } ] }, { "id": "R-HSA-9619756", "name": "NR1H2 binds ABCA1", "equation": "", "summary": "In addition to its well defined role as a transcription factor, liver X receptor \u03b2 (LXR\u03b2 or NR1H2) can directly bind to the C-terminal region of ATP-binding cassette A1 (ABCA1) in the human macrophage-like (THP-1) and human embryonic kidney 293 (HEK293) cell lines to impact ABCA1 protein function (Hozoji M et al. 2008; Hozoji-Inada M et al. 2011). In the absence of cholesterol accumulation in THP-1 cells, the ABCA1:NR1H2 complex stably localizes to the plasma membrane, but apolipoprotein A-I (apoA-I) binding or cholesterol efflux does not occur (Hozoji M et al. 2008; Hozoji-Inada M et al. 2011). Exogenously added NR1H2 ligands, which mimic cholesterol accumulation, cause NR1H2 (LXR\u03b2) to dissociate from ABCA1, thus freeing ABCA1 for apoA-I binding and subsequent cholesterol efflux (Hozoji M et al. 2008; Hozoji-Inada M et al. 2011). Photoaffinity labeling experiments with 8-azido-[\u03b1-(32)P]ATP suggested that the interaction of NR1H2 (LXR\u03b2) with ABCA1 inhibits ATP binding by ABCA1 (Hozoji-Inada M et al. 2011).", "cellular_location": "cytosol, plasma membrane", "input_participant_list": [], "output_participant_list": [], "enzyme_list": [ "O95477-1" ], "evidence": [ { "id": "R-HSA-9619756", "database": "Reactome", "url": "https://www.reactome.org/PathwayBrowser/#R-HSA-9619756" } ] } ], "reaction_participants": [ { "participant_id": "R-ALL-171142", "participant_name": "PL [plasma membrane]", "crossref": [ { "id": "16247", "database": "ChEBI", "url": "" }, { "id": "16247", "database": "ChEBI", "url": "" }, { "id": "16247", "database": "ChEBI", "url": "" }, { "id": "16247", "database": "ChEBI", "url": "" } ] }, { "participant_id": "R-ALL-216770", "participant_name": "PL [transport vesicle membrane]", "crossref": [ { "id": "16247", "database": "ChEBI", "url": "" }, { "id": "16247", "database": "ChEBI", "url": "" 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