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Abstract
ABSTRACTCongenital diaphragmatic hernia (CDH) is a malformation leading to pulmonary hypoplasia, which can be treated in utero by fetal tracheal occlusion (TO). However, the changes of gene expression induced by TO remain largely unknown but could be used to further improve the clinically used prenatal treatment of this devastating malformation. Therefore, we aimed to investigate the pulmonary transcriptome changes caused by surgical induction of diaphragmatic hernia (DH) and additional TO in the fetal rabbit model. Induction of DH was associated with 378 upregulated genes compared to controls when allowing a false-discovery rate (FDR) of 0.1 and a fold change (FC) of 2. Those genes were again downregulated by consecutive TO. But DH+TO was associated with an upregulation of 157 genes compared to DH and controls. When being compared to control lungs, 106 genes were downregulated in the DH group and were not changed by TO. Therefore, the overall pattern of gene expression in DH+TO is more similar to the control group than to the DH group. In this study, we further provide a database of gene expression changes induced by surgical creation of DH and consecutive TO in the rabbit model. Future treatment strategies could be developed using this dataset. We also discuss the most relevant genes that are involved in CDH.
Highlights
The prevalence of congenital diaphragmatic hernia (CDH) ranges between 1-4/10,000 births, which translates to 542 to 2,168 children in EU-27 every year (2008) (Kotecha et al 2012)
Induction of DH was associated with 378 up-regulated genes compared to controls when allowing a false discovery rate (FDR) of 0.1 and a Fold Change (FC) of 2
In this study we further provide a database of gene expression changes induced by surgical creation of DH and consecutive tracheal occlusion (TO) in the rabbit model
Summary
The prevalence of congenital diaphragmatic hernia (CDH) ranges between 1-4/10,000 births, which translates to 542 to 2,168 children in EU-27 every year (2008) (Kotecha et al 2012). Lungs of babies with CDH have fewer and less mature airway branches, a smaller cross-sectional area of pulmonary vessels, remodelled vascular architecture and an altered vasoreactivity (Kinsella et al 2005). At birth, this leads to respiratory insufficiency and persistent pulmonary hypertension (PPHT). This is lethal in up to 30% of cases, despite prenatal referral to high volume centers that offer standardized neonatal care (Grushka et al, 2009; Hayakawa et al, 2013; van den Hout et al, 2011)
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