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

Figure 6.

Figure 6.

MIAT participates in smooth muscle cell transdifferentiation into inflammatory macrophage-like cells through KLF4 activation. A, Expression of SMCs, phagocytosis and/or macrophage markers in hCASMCs stimulated with oxLDL and with or without MIAT knockdown (KD). B, Expression of MIAT, transcription factor KLF4, coeffectors ELK1 and HDAC2 in hCASMCs stimulated with oxLDL and with or without MIAT KD. C, Left, Immunostaining of KLF4 in hCASMCs stimulated with oxLDL and with or without MIAT KD; Right, fluorescence quantification. D, Interaction of Miat/MIAT with Klf4/KLF4 promoter as predicted by LongTarget v2.1. Peaks indicate predicted binding sites of Miat/MIAT within Klf4/KLF4 promoter region. E, Luciferase reporter assay with human KLF4 promoter on oxLDL stimulation/MIAT KD in hCASMCs. F, Luciferase reporter assay with murine Klf4 promoter (containing Miat predicted binding sites; Klf4 promoter_Miat) or promoter flanking regions (harboring no predicted Miat binding sites; Ctrl) in mouse aortic SMCs on Miat overexpression (pCAG-Miat, murine). Bar=50 µm. Data were analyzed by 1-way ANOVA.*P<0.05; **P<0.01; ***P<0.001; ****P<0.0001; P value >0.05 indicates no significance. ctrl indicates control; DAPI, 4′,6-diamidino-2-phenylindole; FC, fibrous cap; hCASMC, human carotid smooth muscle cell; KLF4, Krüppel-like factor 4; oxLDL, oxidized low-density lipoprotein; Rel., relative; and SMC, smooth muscle cell.