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Whole human genome expression analysis on left ventricular free wall heart tissue samples (Dilated Cardiomyopathy)

ABSTRACT: Human left ventricular free wall heart tissue was obtained from end-stage heart failure patients at the moment of heart transplantation

ORGANISM(S): Homo sapiens

PROVIDER: GSE111544 | GEO | 2018/03/08

REPOSITORIES: GEO

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Whole human genome expression analysis on left ventricular free wall heart tissue samples

Project description:Human left ventricular free wall heart tissue was obtained from end-stage heart failure patients at the moment of heart transplantation Left ventricular free wall samples were also obtained from healthy hearts of organ donors, which were not used for transplantation due to size mismatch with available recipients.

2017-09-30 | GSE84796 | GEO

Whole human genome expression analysis on left ventricular free wall heart tissue samples (Dilated Cardiomyopathy)

Project description:Whole human genome expression analysis on left ventricular free wall heart tissue samples (Dilated Cardiomyopathy)

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Changes in molecular profiles of the left ventricle during progressive dilated cardiomyopathy linked heart failure

Project description:To investigate molecular profiles of progressive heart failure, we studied mice that lack expression of the muscle LIM protein (MLPKO). These mice showed dramatic HF progression between three and six weeks of age. We then performed gene expression profile analysis using data obtained from RNA-seq of mid wall left ventricular heart tissue from MLPKO mice and wild-type (WT) controls at three, six, and ten weeks of age (n=3 per group).

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Mutations in the NOTCH pathway regulator MIB1 cause left ventricular noncompaction cardiomyopathy

Project description:Left ventricular noncompaction (LVNC) Causes prominent ventricular trabeculations and reduces cardiac systolic function. The clinical presentation of LVNC ranges from asymptomatic to heart failure. We show that germline mutations in human MIB1 (mindbomb homolog 1), which encodes an E3 ubiquitin ligase that promotes endocytosis of the NOTCH ligands DELTA and JAGGED, cause LVNC in autosomal-dominant pedigrees, with affected individuals showing reduced NOTCH1 activity and reduced expression of target genes. Functional studies in cells and zebrafish embryos and in silico modeling indicate that MIB1 functions as a dimer, which is disrupted by the human mutations. Targeted inactivation of Mib1 in mouse myocardium causes LVNC, a phenotype mimicked by inactivation of myocardial Jagged1 or endocardial Notch1. Myocardial Mib1 mutants show reduced ventricular Notch1 activity, expansion of compact myocardium to proliferative, immature trabeculae and abnormal expression of cardiac development and disease genes. These results implicate NOTCH signaling in LVNC and indicate that MIB1 mutations arrest chamber myocardium development, preventing trabecular maturation and compaction. RNA was isolated from the ventricles of 16 WT and 16 Mib1flox; CTnT-cre hearts at E14.5 and then pooled into four replicates.

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Mutations in the NOTCH pathway regulator MIB1 cause left ventricular noncompaction cardiomyopathy

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Ribo-seq of murine left ventricular tissues

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