Fig. 8
Experimental verification of the expression of hub genes in cardiac injury. A H9c2 cells treated with DMSO or 60 μM isoproterenol for 24 h were performed to analyze mRNA expression levels of hub genes. Values represent means ± SD (n = 3 biologically independent samples). B–Q Characterization of physiological and cardiac features of transverse aortic constriction (TAC) induced heart failure and confirmation of hub genes expression. Heart failure was induced by TAC at a 0.44 mm diameter for 8 weeks. Cardiac function (B and C) was determined in the heart. Hearts were collected and processed for anatomical and histologic analysis. Heart weight/body weight (D) and heart weight/tibia length (E). F Representative image of whole heart, and histological picture of H&E staining, Sirius red staining, and fluorescence-conjugated wheat germ agglutinin (WGA) staining for heart. Bars, 50 μm. Quantification for collagen deposition (G) and cardiomyocyte cross-sectional areas (H). I The levels of malondialdehyde (MDA) in heart lysates. J Apoptosis was determined based on caspase-3 activity. K The expression levels of mRNA of hub genes were confirmed in sham and TAC mice. Values represent means ± SD (n = 4 mice). L–Q Correlations between Ccr5, Csf1r, and Tlr7 mRNA expression levels and cardiac functional parameters. R denotes the correlation coefficient between the variables and P denotes the statistical P-value between the variables, which were obtained by Pearson correlation analysis. All qPCR graphs show gene expression normalized to Glyceraldehyde-3-phosphate dehydrogenase (Gapdh). *P < 0.05; **P < 0.01; ns, no significance