Aim: We hypothesized that polymorphisms in the region encoding for the second transmembrane spanning domain of the epithelial sodium channel may be one factor in the pathogenesis of transient tachypnoea of the newborn...Aim: We hypothesized that polymorphisms in the region encoding for the second transmembrane spanning domain of the epithelial sodium channel may be one factor in the pathogenesis of transient tachypnoea of the newborn. We thus searched for polymorphisms in this region in neonates with transient tachypnoea of the newborn. We also investigated samples from preterm neonates with respiratory distress syndrome, as dysfunction of the epithelial sodium channel might also increase the risk for developing respiratory distress syndrome and in fluence its course. Methods: We used denaturing gradient gel electrophoresis to detect sequence variants in exon 12 and 13 of the epithelial sodium channel. Forty-three neonates with transient tachypnoea of the newborn (gestational age mean± SD : 38.3± 1.2 completed weeks; birthweight: 3088± 426 g), 57 neonates with RDS (gestational age: 29.6 ± 3.5 completed weeks; birthweight: 1272 ± 638 g), and 50 healthy controls were enrolled prospectively. Results: We did not detect any polymorphism. Neither did confirmative sequencing of this region in 16 neonates with transient tachypnoea of the newborn reveal any polymorphism. Conclusion: We conclude that reasons other than polymorphisms in the second transmembrane spanning domain cause transient tachypnoea of the newborn.展开更多
目的探讨PI3K/Akt信号通路对急性肺损伤(ALI)大鼠肺泡上皮钠通道(ENaC)α、β和γ亚基表达的影响。方法成年SD大鼠随机分为对照组、ALI组(脂多糖)、胰岛素组及渥曼青霉素组,每组5只。观察肺组织病理改变,收集支气管肺泡灌洗液(BALF),测...目的探讨PI3K/Akt信号通路对急性肺损伤(ALI)大鼠肺泡上皮钠通道(ENaC)α、β和γ亚基表达的影响。方法成年SD大鼠随机分为对照组、ALI组(脂多糖)、胰岛素组及渥曼青霉素组,每组5只。观察肺组织病理改变,收集支气管肺泡灌洗液(BALF),测量总肺水含量,RT-PCR和Western blot测定ENaC mRNA和蛋白、p-Akt表达。结果胰岛素组BALF蛋白含量、髓过氧化物酶(MPO)活性、总肺水含量较ALI组显著减少(P<0.05),渥曼青霉素组BALF蛋白含量、MPO活性及总肺水含量较胰岛素组显著增加(P<0.05)。ALI组α-、β-和γ-ENaC蛋白表达显著低于对照组(0.33±0.06 vs 1.27±0.07,0.18±0.04 vs 0.72±0.04,0.37±0.04 vs 0.69±0.05)(P<0.05)。胰岛素组蛋白表达α-ENaC(2.19±0.04)、β-ENaC(1.18±0.07)和γ-ENaC(1.18±0.08)显著高于ALI组(P<0.05)。渥曼青霉素组蛋白表达α-ENaC(0.86±0.09)、β-ENaC(0.58±0.05)和γ-ENaC(0.59±0.02)显著低于胰岛素组(P<0.05)。胰岛素组ENaC mRNA和p-Akt较ALI组显著升高(P<0.05)。渥曼青霉素组ENaC mRNA和p-Akt较胰岛素组显著降低(P<0.05)。结论激活PI3K/Akt通路上调3种ENaC亚基表达,从而清除肺水肿液。展开更多
基金This work was supported by the Strategic Program of the Chinese University of Hong Kong and the South China National Research Center for Integrated Biosciences in Collaboration with Zhongshan University.
文摘Aim: We hypothesized that polymorphisms in the region encoding for the second transmembrane spanning domain of the epithelial sodium channel may be one factor in the pathogenesis of transient tachypnoea of the newborn. We thus searched for polymorphisms in this region in neonates with transient tachypnoea of the newborn. We also investigated samples from preterm neonates with respiratory distress syndrome, as dysfunction of the epithelial sodium channel might also increase the risk for developing respiratory distress syndrome and in fluence its course. Methods: We used denaturing gradient gel electrophoresis to detect sequence variants in exon 12 and 13 of the epithelial sodium channel. Forty-three neonates with transient tachypnoea of the newborn (gestational age mean± SD : 38.3± 1.2 completed weeks; birthweight: 3088± 426 g), 57 neonates with RDS (gestational age: 29.6 ± 3.5 completed weeks; birthweight: 1272 ± 638 g), and 50 healthy controls were enrolled prospectively. Results: We did not detect any polymorphism. Neither did confirmative sequencing of this region in 16 neonates with transient tachypnoea of the newborn reveal any polymorphism. Conclusion: We conclude that reasons other than polymorphisms in the second transmembrane spanning domain cause transient tachypnoea of the newborn.
文摘目的探讨PI3K/Akt信号通路对急性肺损伤(ALI)大鼠肺泡上皮钠通道(ENaC)α、β和γ亚基表达的影响。方法成年SD大鼠随机分为对照组、ALI组(脂多糖)、胰岛素组及渥曼青霉素组,每组5只。观察肺组织病理改变,收集支气管肺泡灌洗液(BALF),测量总肺水含量,RT-PCR和Western blot测定ENaC mRNA和蛋白、p-Akt表达。结果胰岛素组BALF蛋白含量、髓过氧化物酶(MPO)活性、总肺水含量较ALI组显著减少(P<0.05),渥曼青霉素组BALF蛋白含量、MPO活性及总肺水含量较胰岛素组显著增加(P<0.05)。ALI组α-、β-和γ-ENaC蛋白表达显著低于对照组(0.33±0.06 vs 1.27±0.07,0.18±0.04 vs 0.72±0.04,0.37±0.04 vs 0.69±0.05)(P<0.05)。胰岛素组蛋白表达α-ENaC(2.19±0.04)、β-ENaC(1.18±0.07)和γ-ENaC(1.18±0.08)显著高于ALI组(P<0.05)。渥曼青霉素组蛋白表达α-ENaC(0.86±0.09)、β-ENaC(0.58±0.05)和γ-ENaC(0.59±0.02)显著低于胰岛素组(P<0.05)。胰岛素组ENaC mRNA和p-Akt较ALI组显著升高(P<0.05)。渥曼青霉素组ENaC mRNA和p-Akt较胰岛素组显著降低(P<0.05)。结论激活PI3K/Akt通路上调3种ENaC亚基表达,从而清除肺水肿液。
