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. 2022 Sep 15;13:5409. doi: 10.1038/s41467-022-33152-9

Fig. 2. The liver-specific C3 deletion rescues pulmonary artery constriction (PAC)-induced right ventricular dysfunction in mice.

Fig. 2

a, b Measured values obtained from the echocardiogram in α-myosin heavy chain promoter-driven Cre (αMHC-Cre) PAC, and albumin promoter-driven Cre (Alb-Cre) PAC, C3 floxed αMHC-Cre (C3fl/fl αMHC-Cre) PAC, and C3 floxed Alb-Cre (C3fl/fl Alb-Cre) PAC mice (n = 3, a p = 0.0002, p < 0.0001, b p = 0.0015, p = 0.0147). The right ventricle (RV) contractile function (right ventricular fractional shortening [RV FS]) and RV size (right ventricular end-diastolic diameter [RVDd]) were evaluated. Data are presented as mean ± standard deviation (SD). c Representative images of Azan staining of the heart in C3fl/fl αMHC-Cre PAC mice (n = 3). d Representative images of Azan staining of the heart in C3fl/fl Alb-Cre PAC mice. LV, left ventricle (n = 3). e, f Quantified fibrotic area of the RV and LV in C3fl/fl αMHC-Cre and C3fl/fl Alb-Cre PAC model mice (n = 3, p = 0.0005, p = 0.039). Data are presented as mean ± SD. gj qRT-PCR analysis of the expression of heart failure markers (Nppb and Myh7) and fibrotic markers (Col3a1 and Ccn2) in the LV, ventricular septum, and RV of αMHC-Cre PAC, and Alb-Cre PAC, C3fl/fl αMHC-Cre PAC, and C3fl/fl Alb-Cre PAC mice (n = 3, g p < 0.0001, p = 0.0003, h p < 0.0001, p < 0.0001, i p < 0.0001, p < 0.0001, j p < 0.0001, p = 0.0012). Data are presented as mean ± standard error of the mean. In qRT-PCR analysis, expression of target genes was normalised to that of Gapdh. Significance was assessed using a two-tailed unpaired Student’s t-test. *p < 0.05; **p < 0.01.