Time dependence of volume overload on left ventricular remodeling during preadolescence

ABSTRACT: We reported the RNAseq analyses of left 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 LV free wall at P14 and P21from VO and sham-operated mice revealed that there were 378 differentially expressed genes between VO and sham group at P14, this number decreased to 184 at P21, there were 1374 differentially expressed genes between P21 and P14 sham group, and the number chenged to 1167 at the presence of VO. GO analysis showed that in the VO and sham comparison, the upregulated genes mainly mediated cell−cell junction and the downregulated genes mainly mediated regulation of immune response at P14, and the upregulated genes mainly mediated cell growth, and downregulated genes mainly mediated response to interferon−beta at P21. As expected, in the normal LV development during preadolescence (from P14 to P21), upregulated genes mainly mediated muscle system process and regulation of membrane potential and the downregulated genes mainly mediated regulation of mitotic cell cycle. VO changed the LV development, the upregulated genes mainly mediated regulation of protein catabolic process and the down regulated genes mainly mediated antigen processing and presentation. KEGG pathway analysis revealed that glucagon signaling pathway was upregulated and phagosome pathway and chemokine signaling pathway were downregulated between VO and sham group at P14, protein processing in endoplasmic reticulum was upregulated and antigen processing and presentation were downregulated at P21 between VO and sham group. In the normal LV development, calcium signaling pathway and cardiac muscle contraction pathway were upregulated while VO changed that to the arginine and proline metabolism . All the above changes were further confirmed by the functional tests.

ORGANISM(S): Mus musculus

PROVIDER: GSE186968 | GEO | 2022/04/07

REPOSITORIES: GEO