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. 2021 Oct 14;144(19):1567–1583. doi: 10.1161/CIRCULATIONAHA.120.052023

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© 2021 The Authors.

Circulation is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 5. — MIAT triggers inflammation and macrophage activity in advanced atherosclerotic lesions. A, Expression of MIAT in human monocyte-derived macrophages on MIAT knockdown (KD). B, Uptake of florescence-labeled oxLDL in human monocyte-derived macrophages on MIAT KD monitored through live-cell imaging and analyzed by 1-way ANOVA. C, Expression of MIAT in human monocyte-derived macrophages on stimulation with oxLDL. D and E, Expression of MIAT in THP1-derived macrophages stimulated with LPS (D) or IL4 (E). F, Immunostaining of NF-κB in human monocyte-derived macrophages on oxLDL stimulation with or without MIAT KD. Quantification is shown on the right side. G, Binding of endogenous MIAT to NFKB2/p52/p100 in THP1 cells. MIAT expression in THP1 cells was triggered by oxLDL stimulation and immunoprecipitation with NFKB2/p52/p100 or control IgG performed. MIAT or GAPDH (as unrelated target) enrichment in NFKB2 IP fraction were quantified with real-time quantitative polymerase chain reaction. Data were analyzed by Student t test (A, C–E, G), AUC (B), or Mann-Whitney U test (F). Bar=50 µm. **P<0.01; ***P<0.001; ****P<0.0001. ctrl indicates control; DAPI, 4′,6-diamidino-2-phenylindole; FITC, fluorescein isothiocyanate; IgG, immunoglobulin G; IL4, interleukin 4; IP, immunoprecipitation; LPS, lipopolysaccharide; NF-κB, Nuclear Factor κ-light-chain enhancer of activated B cells; oxLDL, oxidized low-density lipoprotein; and Rel., relative.