ArticleJournal of pediatric surgery2010
Spatiotemporal alteration in phosphatidylinositide 3-kinase-serine/threonine protein kinase B signaling in the nitrofen-induced hypoplastic lung.
Article in Journal of pediatric surgery, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Malarial PI4K inhibitor induced diaphragmatic hernias in rat: Potential link with mammalian kinase inhibition.Birth defects research · 2022Article
- The transcriptome of nitrofen-induced pulmonary hypoplasia in the rat model of congenital diaphragmatic hernia.Pediatric research · 2016Article
- Prenatal administration of retinoic acid upregulates connective tissue growth factor in the nitrofen CDH model.Pediatric surgery international · 2011Article
- Prenatal retinoic acid treatment upregulates late gestation lung protein 1 in the nitrofen-induced hypoplastic lung in late gestation.Pediatric surgery international · 2011Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
purposeThe pathogenesis of pulmonary hypoplasia in congenital diaphragmatic hernia (CDH) is not fully understood. The serine/threonine protein kinase B (AKT) plays important roles for lung morphogenesis through epithelial-mesenchymal interaction in phosphatidylinositide 3-kinase (PI3K)-dependent manner. It has been reported that the lung explant morphogenesis in mice is interfered by inhibitors of the PI3K-AKT pathway. We hypothesized that PI3K and AKT gene and protein expression/distribution are altered during epithelial morphogenesis in the nitrofen-induced hypoplastic lung.
methodsPregnant rats were exposed to either olive oil or nitrofen on day 9 of gestation (D9). Fetal lungs were harvested on D15, D18, and D21 and divided into 3 groups as follows: control, nitrofen with CDH (CDH[-]), and nitrofen without CDH (CDH[+]) (n = 8 at each time-point, respectively). Reverse transcription polymerase chain reaction and immunohistochemistry were performed.
resultsMessenger RNA expression levels of PI3K at D21 was significantly decreased in CDH(-) and CDH(+) group (5.71 +/- 0.85 and 6.80 +/- 0.88, respectively) compared to controls (8.95 +/- 3.22; P < .05). Messenger RNA levels of AKT were also significantly decreased at D18 in CDH(-) and CDH(+) lungs (1.21 +/- 0.16 and 1.20 +/- 0.32, respectively) compared to controls (1.62 +/- 0.14; P < .01). The PI3K immunoreactivity was diminished in the distal epithelium at D18 and decreased in the overall intensity at D21 in hypoplastic lungs compared to controls. The AKT immunoreactivity was decreased in mesenchyme at D18 and decreased overall intensity at D21 in CDH lungs compared to controls.
conclusionSpatiotemporal alteration of pulmonary PI3K and AKT gene and protein expression during epithelial morphogenesis may interfere with epithelial-mesenchymal interaction, causing pulmonary hypoplasia in CDH by disrupting PI3K-AKT signaling pathway.
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