Gene expression of fibroblast growth factors 10 and 7 is downregulated in the lung of nitrofen-induced diaphragmatic hernia in rats

Teramoto, Honami; Yoneda, Akihiro; Puri, Prem

doi:10.1016/s0022-3468(03)00183-0

Cited by 55 publications

(37 citation statements)

References 16 publications

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“…Fgf10 null mice display complete disruption of mainstem bronchus as well as all subsequent pulmonary branching morphogenesis [23]. It has also been reported that pulmonary mRNA expression level of Fgf10 is significantly decreased in the nitrofen CDH model compared to controls [24].…”

Section: Discussionmentioning

confidence: 93%

Up-regulation of Wnt5a gene expression in the nitrofen-induced hypoplastic lung

Doi¹,

Puri²

2009

Journal of Pediatric Surgery

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Section: Discussionmentioning

confidence: 93%

Up-regulation of Wnt5a gene expression in the nitrofen-induced hypoplastic lung

Doi¹,

Puri²

2009

Journal of Pediatric Surgery

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“…Chang et al [123] recently showed a downregulation of VEGF expression in the nitrofen-induced rat model of CDH. FGF7 and FGF10 have also been shown to be downregulated in the same model [124] . Furthermore, pulmonary Shh expression in human CDH is delayed, peaking in the canalicular/saccular period as opposed to its peak in the pseudoglandular phase in normal development [125] .…”

Section: Congenital Diaphragmatic Herniamentioning

confidence: 86%

The Molecular Basis for Abnormal Human Lung Development

2005

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Our understanding of lung development in the past two decades has moved from an anatomical to a histological basis and, most recently, to a molecular basis. Tissue interactions specify tracheal and lung primordia formation, program branching morphogenesis of the airway epithelium and regulate epithelial differentiation. In addition, lung development is influenced by mechanical and humoral factors. The regulatory molecules involved in morphogenetic signaling include growth and transcription factors and extracellular matrix molecules. These morphogenetic signals are responsible for lung patterning and differentiation. We will provide a brief overview of molecular signaling during early respiratory formation, airway branching, pulmonary vascularization and epithelial differentiation. We will then review aberrant morphogenetic signaling in human lung abnormalities, such as tracheoesophageal fistula, congenital diaphragmatic hernia, pulmonary hyperplasia, alveolar capillary dysplasia, congenital cystic adenomatoid malformation and bronchopulmonary dysplasia.

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“…It has also been shown that NKCC-1 activates mitogen-activated protein kinase in fibroblasts [50] and is itself stimulated by fibroblast growth factor (FGF) [51]. FGF enhances the contraction rates and growth of airway smooth muscle [45] and hypoplastic lungs show remedial growth when treated with FGF [52,53]. Considering our results that NKCC-1 is significantly decreased in CDH-affected hypoplastic lungs, it could be speculated that NKCC-1 plays a role in normal lung growth not only by being a chloride transporter taking part in secretion, but also through a more direct mitogenic effect.…”

Section: Discussionmentioning

confidence: 99%

NKCC-1 and ENaC are down-regulated in nitrofen-induced hypoplastic lungs with congenital diaphragmatic hernia

et al. 2008

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Congenital diaphragmatic hernia (CDH) is accompanied by pulmonary hypoplasia and pulmonary hypertension. Fetal lung growth is dependent on the secretion of lung liquid, which normally is absorbed at partus. The ion channel NKCC-1 is involved in this secretory process, but has recently also been reported to be implicated in absorption. CDH patients show a disturbed transition from secretion to absorption. alpha- and beta-ENaC are essential for lung liquid absorption. Common for all transcellular ion transport is the need for Na/K-ATPase as a primary driving force. The aim of the study was first to map the normal pulmonary expression of the above proteins during late gestation and secondly to see if the expression was affected in a CDH rat model. Pregnant Sprague-Dawley rat dams were given nitrofen on gestational day 9.5 to induce CDH. The fetuses were removed on gestational days E18 and E21. In addition, newborn rats were harvested postpartum on day P2. The fetuses were put into one of two groups: hypoplastic lungs without CDH (N-CDH) and hypoplastic lungs with CDH (N+CDH). The pulmonary expression of NKCC-1, alpha-/beta-ENaC and Na/K-ATPase was then analyzed using Western blot. We found that the protein levels of NKCC-1 on gestational days E18 and E21 were significantly lower among fetuses with N+CDH as well as N-CDH compared to controls. The expression of beta-ENaC was also significantly down-regulated in both the groups on E18 and E21. The protein levels of alpha-ENaC and Na/K-ATPase were not found to be significantly decreased, but both showed a tendency towards down-regulation. The marked down-regulation of NKCC-1 in fetal hypoplastic lungs with CDH indicates a possibly decreased lung liquid production. This may be one of the mechanisms behind the disturbed pulmonary development in CDH. We also show that beta-ENaC is down-regulated. Down-regulation of beta-ENaC may result in abnormal lung liquid absorption, which could be one of the mechanisms behind the respiratory distress seen in CDH patients postpartum.

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Gene expression of fibroblast growth factors 10 and 7 is downregulated in the lung of nitrofen-induced diaphragmatic hernia in rats

Cited by 55 publications

References 16 publications

Up-regulation of Wnt5a gene expression in the nitrofen-induced hypoplastic lung

Up-regulation of Wnt5a gene expression in the nitrofen-induced hypoplastic lung

The Molecular Basis for Abnormal Human Lung Development

NKCC-1 and ENaC are down-regulated in nitrofen-induced hypoplastic lungs with congenital diaphragmatic hernia

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