Project description:Tetralogy of Fallot (TOF) is one of the most common heart defects in children and the underlying mechanisms remain elusive. miRNAs are a recently discovered class of regulators of gene expression and are becoming increasingly recognized as important regulators of heart development and function. The objective of the present study was to identify miRNAs that are abnormally expressed in clinical infant outflow tract myocardium tissues of TOFs. Microarray was used to analyze miRNA expression profiles in infant outflow tract myocardium tissues of TOFs and paired normal ones.
Project description:Tetralogy of Fallot (TOF) is one of the most common heart defects in children and the underlying mechanisms remain elusive. miRNAs are a recently discovered class of regulators of gene expression and are becoming increasingly recognized as important regulators of heart development and function. The objective of the present study was to identify miRNAs that are abnormally expressed in clinical infant outflow tract myocardium tissues of TOFs.
Project description:This SuperSeries is composed of the following subset Series: GSE35490: Noncoding RNA expression in myocardium from infants with tetralogy of Fallot [miRNA profiling] GSE35776: Noncoding RNA expression in myocardium from infants with tetralogy of Fallot [mRNA profiling] Refer to individual Series
Project description:Adult right ventricle from Tetralogy of Fallot patients undergoing pulmonary valve replacement vs right ventricle myocardium from unused donor hearts we used Microarray to determine whether there were differences in gene expression between these groups
Project description:Tetralogy of Fallot (TOF) is the most common cyanotic congenital heart defect with a world-wide prevalence of 3 to 4 cases per 10,000 life births. TOF is a congenital heart disease with four major cardiac defects, i.e., ventricular septal defect, overriding aortic root, infundibular stenosis of the pulmonary artery, and right ventricular hypertrophy. Treatment relies on correction surgery in early infancy. This study performed whole genome microarray gene expression profiling of cardiac specimens of the right ventricular outflow tract (RVOT), which were recovered during correction surgery of TOF from 11 pediatric patients diagnosed with TOF cardiac defects.
Project description:To determine cardiac transcription profile in acyanotic Tetralogy of Fallot patients, we collected myocardial samples immediately after institution of cardiopulmonary bypass from acyanotic Tetralogy of Fallot patients undergoing corrective surgery. The transcriptional profile of the mRNA in these samples was measured with gene array technology. Myocardial samples were collected, immediately after institution of cardiopulmonary bypass from acyanotic Tetralogy of Fallot patients undergoing corrective surgery.
Project description:To determine cardiac transcription profile in cyanotic Tetralogy of Fallot patients, we collected myocardial samples immediately after institution of cardiopulmonary bypass from cyanotic Tetralogy of Fallot patients undergoing corrective surgery. The transcriptional profile of the mRNA in these samples was measured with gene array technology. Myocardial samples were collected, immediately after institution of cardiopulmonary bypass from cyanotic Tetralogy of Fallot patients undergoing corrective surgery.
Project description:Congenital heart defects (CHDs) occur in 0.5–1% of live births, yet the underlying genetic etiology remains mostly unknown. Recently, a new source of myocardial cells, namely the second heart field (SHF), was discovered in the splanchnic mesoderm. Abnormal development of the SHF leads to a spectrum of outflow tract defects, such as persistent truncus arteriosus and tetralogy of Fallot. Intracellular Ca2+ signaling is known to be essential formany aspects of heart biology including heart development, but its role in the SHF is uncertain. Here, we analyzed mice deficient for genes encoding inositol 1,4,5-trisphosphate receptors (IP3Rs), which are intracellular Ca2+ release channels on the endo/sarcoplasmic reticulum that mediate Ca2+ mobilization. Mouse embryos that are double mutant for IP3R type 1 and type 3 (IP3R1−/−IP3R3−/−) show hypoplasia of the outflow tract and the right ventricle, reduced expression of specific molecular markers and enhanced apoptosis ofmesodermal cells in the SHF. Gene expression analyses suggest that IP3R-mediated Ca2+ signalingmay involve, at least in part, theMef2C–Smyd1 pathway, a transcriptional cascade essential for the SHF. These data reveal that IP3R type 1 and type 3 may play a redundant role in the development of the SHF. In total 4 samples were analyzed, they represent two different genotypes (wt, double ko) that were tested in duplicate each.
Project description:The right ventricular tissues of 5 children with tetralogy of Fallot and 5 healthy unaffected individuals were collected and sequenced in full transcriptome. Mechanism of tetralogy of fallot and cerna regulatory network were analyzed.
Project description:The right ventricular tissues of 5 children with tetralogy of Fallot and 5 healthy unaffected individuals were collected and sequenced in full transcriptome. Mechanism of tetralogy of fallot and cerna regulatory network were analyzed.
