Fig. 7: NR4a1 knockdown improves the effects of pathological cardiac remodeling and mitochondrial function in vitro. | Nature Communications

Fig. 7: NR4a1 knockdown improves the effects of pathological cardiac remodeling and mitochondrial function in vitro.

From: Semaglutide ameliorates cardiac remodeling in male mice by optimizing energy substrate utilization through the Creb5/NR4a1 axis

Fig. 7

A Immunofluorescence staining and quantification of a-actinin in NRVMs reproducing siRNA/siNR4a1 virus after PE/PBS stimulation (scale bar: 50 μm; n = 3 independent experiments with similar results); F (3, 20) = 86.03, P = 1.3e-011. B The mRNA levels of the myocardial hypertrophy indicators ANP, BNP and β-MHC (scale bar: 50 μm; n = 6); Anp: F (3, 20) = 279.7, P = 1.7e-016; Bnp: F (3, 20) = 149.5, P = 7.3e-014; β-MHC: F (3, 20) = 213.2, P = 2.4e-015. C Representative confocal image of mitochondrial morphology stained by MitoTracker and the quantification of fragmented, intermediate, and elongated mitochondria (scale bar: 50/20 μm; n = 6). D NRVMs transfected with siRNA and siNR4a1 were subjected to an OCR assay. OCR was normalized by the total number of cardiomyocytes in each group (six pore cells per group; n = 6). E ATP production-coupled respiration in D (n = 6); F (3, 20) = 149.7, P = 7.2e-014. All results are shown as the mean ± SEM, and analysis using a one-way ANOVA followed by Bonferroni post hoc test (A–C and E) was conducted. For the analysis in D, repeated measures two-way ANOVA followed by Sidak post hoc test was conducted. p values are indicated. Source data are provided as a Source Data file. PE, phenylephrine; NRVMs, neonatal rat ventricular myocytes; OCR, oxygen consumption rate; FCCP, carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone.

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