Fig. 8: LncBAR enhances cardiomyocyte proliferation and cardiac regeneration by activating BRG1 and PI3K-AKT pathway.

Western blot analysis and quantification of SWI/SNF complex subunits (a, c) and PI3K-AKT pathway activation (a, b, d, e) in apical tissue post-AR injury (n = 3 biological replicates). f Schematic depiction of AR experiments. Viruses harboring LncBAR, shBrg1, or respective controls were intramyocardially injected into neonatal mouse hearts, with PBS as a non-viral control. AR surgery was performed at P8. Echocardiography and histological samples were collected at AR7 and AR21. g RT-qPCR analysis showing the expression level of LncBAR and Brg1 in hearts receiving the virus injection (n = 5 mice). Representative confocal z-stack images and quantification of Ki67+ cTnI+ CMs (h), and pH3+ cTnI+ CMs (i) in apex zone of AR7 hearts. Yellow arrows indicate Ki67+ or pH3+ CMs (n = 15 fields, 3 mice/group). Scale bars, 20 µm. j Representative Masson’s trichrome-stained sagittal heart sections with fibrotic area quantification at AR21 (n = 5 mice). Scale bars, 1 mm. Echocardiography analysis of mouse hearts at AR21. LVEF (k): left ventricular ejection fraction; LVFS (l): left ventricular fractional shortening; LVEDV (m): left ventricular end-diastolic volume; LVESV (n): left ventricular end-systolic volume (n = 6 mice). Data are presented as mean ± SEM. Statistical significance was determined by two-tailed unpaired t test, one-way ANOVA, or two-way ANOVA with Tukey’s multiple comparisons test. *P < 0.05, **P < 0.01, ***P < 0.001.