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首页> 外文期刊>American Journal of Physiology >Novel mechanisms in murine nitrofen-induced pulmonary hypoplasia: FGF-10 rescue in culture.
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Novel mechanisms in murine nitrofen-induced pulmonary hypoplasia: FGF-10 rescue in culture.

机译：小鼠硝苯芬诱导的肺发育不良的新机制：培养物中的FGF-10拯救。

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摘要

We evaluated the role of the key pulmonary morphogenetic gene fibroblast growth factor-10 (Fgf10) in murine nitrofen-induced primary lung hypoplasia, which is evident before the time of diaphragm closure. In situ hybridization and competitive RT-PCR revealed a profound disturbance in the temporospatial pattern as well as a 10-fold decrease in mRNA expression level of Fgf10 but not of the inducible inhibitor murine Sprouty2 (mSpry2) after nitrofen treatment. Exogenous FGF-10 increased branching not only of control lungs [13% (right) and 27% (left); P < 0.01] but also of nitrofen-exposed lungs [23% (right) and 77% (left); P < 0.01]. Expression of mSpry2 increased 10-fold with FGF-10 in both nitrofen-treated and control lungs, indicating intact downstream FGF signaling mechanisms after nitrofen treatment. We conclude that nitrofen inhibits Fgf10 expression, which is essential for lung growth and branching. Exogenous FGF-10 not only stimulates FGF signaling, marked by increased mSpry2 expression, in both nitrofen-treated and control lungs but also substantially rescues nitrofen-induced lung hypoplasia in culture.
机译：我们评估了关键的肺形态发生基因成纤维细胞生长因子10（Fgf10）在小鼠硝苯芬诱导的原发性肺发育不全中的作用，这在隔膜关闭之前很明显。原位杂交和竞争性RT-PCR揭示了颞pat模式的严重紊乱，以及硝基苯酚处理后Fgf10的mRNA表达水平下降了10倍，但诱导抑制剂鼠Sprouty2（mSpry2）却没有。外源性FGF-10不仅增加了对照肺的分支[13％（右）和27％（左）; P <0.01]，但也有暴露于硝基苯的肺[23％（右）和77％（左）; P <0.01]。硝基苯酚处理和对照肺中，mSpry2的表达均用FGF-10增长10倍，表明硝基苯酚处理后完整的下游FGF信号传导机制。我们得出的结论是硝基苯酚抑制Fgf10表达，这对于肺部生长和分支至关重要。外源性FGF-10不仅刺激硝基苯酚处理的肺和对照肺中以mSpry2表达增加为特征的FGF信号传导，而且还基本上可以挽救硝基苯酚诱导的培养中的肺发育不全。

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