Fig. 2: In vivo knockdown of MAARS inhibits atherosclerotic lesion formation.

a LDLR^−/− mice were i.v. injected with vehicle control gapmeR (n = 15) or MAARS gapmeR (n = 13) twice per week (7.5 mg kg⁻¹ per injection per mouse) and placed on HCD for 12 weeks. b Silencing of MAARS was assessed by RT-qPCR in RNA derived from the aortic intima (n = 6 for control gapmeR group and n = 5 for MAARS gapmeR group). c RNA-ISH representative images and quantification of MAARS knockdown in Mac2 co-stained aortic sinus from control and MAARS KD groups of mice. Representative images and quantification for Oil-Red O staining in the lesions of aortic sinus (d) and in the descending aorta (e) of the control (n = 15) and MAARS KD (n = 13) mice. f TUNEL (red) staining was detected in the aortic sinus of the control (n = 15) and MAARS knockdown (KD, n = 13) groups of LDLR^−/− mice fed HC, counterstained with DAPI (blue), and quantified as total red fluorescent staining per lesion area. g The aortic sinus was co-stained with cleaved caspase-3 (red) and Mac-3 antibodies (green) and the Mac3-associated caspase-3 fluorescence was quantified in the aortic sinus of the control (n = 15) and MAARS KD (n = 13) mice. For all panels, values are mean ± SD; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; *****p < 0.00001.