Time dependence of volume overload on right ventricular remodeling during preadolescence

We reported the RNAseq analyses of right ventricualr free wall myocardium in young volume overload (VO) C57/BL6 mice.VO was induced by the fistula between abdominal aorta and inferior vena cava (AVF) on postnatal day 7(P7). RNAseq analyses of RV free wall at P14 and P21from VO and sham-operated mice revealed that there were 981 differentially expressed genes between VO and sham group at P14, this number increased to 1907 at P21, there were 3012 differentially expressed genes between P21 and P14 sham group, and the number increased to 3470 at the presence of VO. GO analysis showed that in the VO and sham comparison, the upregulated genes mainly mediated mitosis and cell division and the downregulated genes mainly mediated heart contraction at P14, and the upregulated genes mainly mediated immune response, and downregulated genes mainly mediated cellular respiration at P21. As expected, in the normal RV development during preadolescence (from P14 to P21), upregulated genes mainly mediated oxidative phosphorylation and cellular respiration and the downregulated genes mainly mediated vasculogenesis. VO changed the RV development, the upregulated genes mainly mediated heart contraction and the down regulated genes mainly mediated vasculogenesis and cell cycle. KEGG pathway analysis revealed that cell cycle pathway was upregulated and cardiac muscle contraction and thyroid hormone signaling pathway were downregulated between VO and sham group at P14, phagosome pathway was upregulated and citrate cycle (TCA) cycle and thermogenesis were downregulated at P21 between VO and sham group. In the normal RV development, TCA cycle and cardiac muscle contraction pathway were upregulated while VO changed that to the upregulations of cardiomyopathy pathways and thyroid hormone signaling pathway. All the above changes were further confirmed by the functional tests. Overall design: RNAseq analyses of right ventricular free wall myocardium in young volume overload and sham-operated C57/BL6 mice