Abstract：
AIMS:Right ventricular failure (RVF) varies significantly from the more common left ventricular failure (LVF). This study was undertaken to determine potential molecular pathways that are important in human right ventricular (RV) function and may mediate RVF. MATERIALS AND METHODS:We analyzed mRNA of human non-failing LV and RV samples and RVF samples from patients with pulmonary arterial hypertension (PAH), and post-LVAD implantation. We then performed transcript analysis to determine differential expression of genes in the human heart samples. Immunoblot quantification was performed followed by analysis of non-failing and failing phenotypes. KEY FINDINGS:Inflammatory pathways were more commonly dysregulated in RV tissue (both non-failing and failing phenotypes). In non-failing human RV tissue we found important differences in expression of FIGF, TRAPPAC, and CTGF suggesting that regulation of normal RV and LV function are not the same. In failing RV tissue, FBN2, CTGF, SMOC2, and TRAPP6AC were differentially expressed, and are potential targets for further study. SIGNIFICANCE:This work provides some of the first analyses of the molecular heterogeneity between human RV and LV tissue, as well as key differences in human disease (RVF secondary to pulmonary hypertension and LVAD mediated RVF). Our transcriptional data indicated that inflammatory pathways may be more important in RV tissue, and changes in FIGF and CTGF supported this hypothesis. In PAH RV failure samples, upregulation of FBN2 and CTGF further reinforced the potential significance that altered remodeling and inflammation play in normal RV function and failure.
journal_name
Life Scijournal_title
Life sciencesauthors
Williams JL,Cavus O,Loccoh EC,Adelman S,Daugherty JC,Smith SA,Canan B,Janssen PML,Koenig S,Kline CF,Mohler PJ,Bradley EAdoi
10.1016/j.lfs.2018.01.021subject
Has Abstractpub_date
2018-03-01 00:00:00pages
118-126eissn
0024-3205issn
1879-0631pii
S0024-3205(18)30027-4journal_volume
196pub_type
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