...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Pediatric Pulmonology >Regulation of pulmonary surfactant synthesis in fetal rat type II alveolar epithelial cells by microRNA-26a
【24h】

Regulation of pulmonary surfactant synthesis in fetal rat type II alveolar epithelial cells by microRNA-26a

机译：microRNA-26a对胎鼠II型肺泡上皮细胞肺表面活性物质合成的调控

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Pulmonary surfactant, a unique developmentally regulated, phospholipid-rich lipoprotein, is synthesized by the type II epithelial cells (AECII) of the pulmonary alveolus, where it is stored in organelles termed lamellar bodies. The synthesis of pulmonary surfactant is under multifactorial control and is regulated by a number of hormones and factors, including glucocorticoids, prolactin, insulin, growth factors, estrogens, androgens, thyroid hormones, and catecholamines acting through beta-adrenergic receptors, and cAMP. While there is increasing evidence that microRNAs (miRNAs) are involved in the regulation of almost every cellular and physiological process, the potential role of miRNAs in the regulation of pulmonary surfactant synthesis remains unknown. miRNA-26a (miR-26a) has been predicted to target SMAD1, one of the bone morphogenetic protein (BMP) receptor downstream signaling proteins that plays a key role in differentiation of lung epithelial cells during lung development. In this study, we explored the regulation role of miR-26a in the synthesis of pulmonary surfactant. An adenoviral miR-26a overexpression vector was constructed and introduced into primary cultured fetal AECII. GFP fluorescence was observed to determinate the transfection efficiency and miR-26a levels were measured by RT-PCR. MTT was performed to analyze AECII viability. qRT-PCR and Western blotting were used to determine the mRNA and protein level of SMAD1 and surfactant-associated proteins. The results showed that miR-26a in fetal AECII was overexpressed after the transfection, and that the overexpression of miR-26a inhibited pulmonary surfactant synthesis in AECII. There was no significant change in cell proliferation. Our results further showed that overexpression of miR-26a reduced the SMAD1 expression both in mRNA and protein level in fetal AECII. These findings indicate that miR-26a regulates surfactant synthesis in fetal AECII through SMAD1.
机译：肺表面活性剂是一种独特的发育调节，富含磷脂的脂蛋白，由肺泡的II型上皮细胞（AECII）合成，并储存在称为层状体的细胞器中。肺表面活性物质的合成受多因素控制，并受多种激素和因子的调节，包括糖皮质激素，催乳激素，胰岛素，生长因子，雌激素，雄激素，甲状腺激素和通过β-肾上腺素受体和cAMP作用的儿茶酚胺。尽管越来越多的证据表明，微小RNA（miRNA）参与了几乎所有细胞和生理过程的调控，但miRNA在调控肺表面活性物质合成中的潜在作用仍然未知。 miRNA-26a（miR-26a）已被预测靶向SMAD1，SMAD1是骨形态发生蛋白（BMP）受体下游信号蛋白之一，在肺发育过程中在肺上皮细胞的分化中起关键作用。在这项研究中，我们探讨了miR-26a在肺表面活性物质合成中的调控作用。构建了腺病毒miR-26a过表达载体，并将其引入原代培养的胎儿AECII中。观察到GFP荧光确定转染效率，并且通过RT-PCR测量miR-26a水平。进行MTT以分析AECII生存力。使用qRT-PCR和Western印迹法确定SMAD1和表面活性剂相关蛋白的mRNA和蛋白水平。结果表明，转染后胎儿AECII中miR-26a过表达，miR-26a过表达抑制AECII中肺表面活性物质的合成。细胞增殖没有明显变化。我们的结果进一步表明，miR-26a的过表达降低了胎儿AECII mRNA和蛋白水平的SMAD1表达。这些发现表明，miR-26a通过SMAD1调节胎儿AECII中的表面活性剂合成。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号