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Nicotine stimulates branching and expression of SP-A and SP-C mRNAs in embryonic mouse lung culture.

机译:尼古丁刺激胚胎小鼠肺培养物中SP-A和SP-C mRNA的分支和表达。

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摘要

Although the effects of maternal smoking on fetal growth and viability are overwhelmingly negative, there is a paradoxical enhancement of lung maturation as evidenced, in part, by a lower incidence of respiratory distress syndrome in infants of smoking mothers. Other epidemiologic and experimental evidence further support the view that a tobacco smoke constituent, possibly nicotine, affects the development of the lung in utero. We are studying the direct effects of nicotine on murine lung development using a serumless organ culture system. We have found that embryonic lungs explanted at 11 days gestation showed a 32% increase in branching after 4 days in culture in the presence of 1 microM nicotine and 7- to 15-fold increases in mRNAs encoding surfactant proteins A and C after 11 days. The effect of nicotine exposure on surfactant gene expression is apparently mediated by nicotinic acetylcholine receptors because it was blocked by D-tubocurarine. The nicotine-induced stimulation of surfactant gene expression could, in part, account for the effect of maternal smoking on the incidence of respiratory distress syndrome.
机译:尽管孕妇吸烟对胎儿生长和生存能力的影响绝大多数是负面的,但有一部分吸烟的母亲患呼吸窘迫综合征的发生率较低,这证明了肺成熟的反常增强。其他流行病学和实验证据进一步支持以下观点:烟草烟雾成分(可能是尼古丁)会影响子宫内肺的发育。我们正在研究使用无血清器官培养系统对烟碱对鼠肺发育的直接影响。我们发现,在妊娠1天后第11天移植的胚胎肺在培养1天后存在1 microM尼古丁的情况下培养4天后分支增加了32%,而在11天后编码表面活性剂蛋白A和C的mRNA表达增加了7至15倍。烟碱暴露对表面活性剂基因表达的影响显然是由烟碱乙酰胆碱受体介导的,因为它被D-微管尿素所阻断。尼古丁诱导的表面活性剂基因表达的刺激可以部分解释母体吸烟对呼吸窘迫综合征发生率的影响。

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