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首页> 外文期刊>Journal of Pediatric Surgery: Official Journal of the Surgical Section of the American Academy of Pediatric, the British Association of Paediatric Surgeons, the American Pediatric Surgical Association, and the Canadian Association of Paediatric Surgeons >Reduced expression of aquaporin 5 water channel in nitrofen-induced hypoplastic lung with congenital diaphragmatic hernia rat model.
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Reduced expression of aquaporin 5 water channel in nitrofen-induced hypoplastic lung with congenital diaphragmatic hernia rat model.

机译：先天性diaphragm肌疝大鼠模型中水通道蛋白5水通道在硝基芬诱导的增生性肺中的表达降低。

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PURPOSE: Pulmonary hypoplasia remains the principal cause of high morbidity and mortality in patients with congenital diaphragmatic hernia (CDH). The precise mechanisms causing lung hypoplasia remains unclear. Aquaporins (AQPs) are reported to constitute a family of water channels that facilitate membrane water permeability in various tissues of animals. Aquaporin 5 has been reported to be an important marker expressed in type I alveolar epithelial cells in late gestation and mediates water transport across the human airway epithelium. We hypothesized that AQP5 is reduced in hypoplastic lungs and therefore designed this study to determine AQP5 expression in normal and hypoplastic lungs. METHODS: Fetal rat lungs of control (n=23) and nitrofen-treated (n=37) dams were harvested on embryonic day (E) 15, E17, E19, and E21. The expression of the AQP5 was analyzed in each lung by real-time reverse transcriptase-polymerase chain reaction. Immunohistochemical studies were performed to evaluate the protein expression level of AQP5. RESULTS: Aquaporin 5 messenger RNA levels on E21 were significantly reduced in lungs from the nitrofen with CDH group (11.8 +/- 2.3) compared with normal controls (23.5 +/- 11.8) and nitrofen without CDH group (26.9 +/- 13.0) (P < .05). Aquaporin 5 immunohistochemistry demonstrated AQP5 strongly expressed at the apical membrane of type I alveolar epithelial cells in the normal and nitrofen without CDH groups. By contrast, the AQP5-positive cells were markedly reduced in hypoplastic lungs in the nitrofen with CDH group. CONCLUSION: Our results show that the expression of AQP5 is down-regulated in hypoplastic lungs with CDH. Down-regulation of AQP5 may result in abnormal pulmonary fluid metabolism in perinatal period and may be one of the mechanisms disturbing the pulmonary development in late stage in the CDH model.
机译：目的：肺发育不全仍然是先天性diaphragm肌疝（CDH）患者高发病率和高死亡率的主要原因。导致肺发育不全的确切机制仍不清楚。据报道水通道蛋白（AQP）构成水通道家族，其促进动物各种组织中的膜水渗透性。据报道水通道蛋白5是在妊娠晚期在I型肺泡上皮细胞中表达的重要标志物，并介导水在人类气道上皮中的运输。我们假设AQP5在增生性肺中减少，因此设计了该研究以确定正常和增生性肺中AQP5的表达。方法：在胚胎第（E）15，E17，E19和E21日收获对照组（n = 23）和硝基苯酚处理（n = 37）大坝的胎鼠肺。通过实时逆转录酶-聚合酶链反应分析每个肺中AQP5的表达。进行了免疫组织化学研究以评估AQP5的蛋白表达水平。结果：与正常对照组（23.5 +/- 11.8）和不具有CDH组的硝基苯酚（26.9 +/- 13.0）相比，CDH组的硝基苯酚（11.8 +/- 2.3）和非CDH组的硝基苯酚（26.9 +/- 13.0）的肺中E21上水通道蛋白5信使RNA的水平明显降低（P <.05）。 Aquaporin 5免疫组织化学表明，AQP5在正常人和不含CDH组的nitrofen中在I型肺泡上皮细胞的顶膜强烈表达。相比之下，CDH组硝基苯酚的增生性肺中AQP5阳性细胞明显减少。结论：我们的结果表明，CDH在增生性肺中AQP5的表达下调。 AQP5的下调可能会导致围产期肺液代谢异常，并且可能是CDH模型后期扰乱肺发育的机制之一。

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