SP-B deficiency causes respiratory failure in adult mice
SP-B deficiency causes respiratory failure in adult mice
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DOI：
10.1152/ajplung.00011.2003
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发表时间：
2003-09-01
影响因子：
4.9
通讯作者：
Weaver, TE
中科院分区：
文献类型：
--
作者：
Melton, KR;Nesslein, LL;Weaver, TE
表面活性剂蛋白(SP)-B位点的靶向缺失会导致小鼠新生儿致命的呼吸窘迫。为了评估SP-B对出生后肺功能的重要性，在SP-B-/-小鼠中，在外源性多西环素控制下有条件地表达小鼠SP-B cDNA，建立了复合转基因小鼠。强力霉素调节SP-B的表达完全纠正了复合SP-B-/-小鼠的肺功能，并保护小鼠免于出生时呼吸衰竭。对成年复方SP-B-/-小鼠停用强力霉素可导致SP-B肺泡含量降低，SP-B浓度降低至时引起呼吸衰竭
Targeted deletion of the surfactant protein (SP)-B locus in mice causes lethal neonatal respiratory distress. To assess the importance of SP-B for postnatal lung function, compound transgenic mice were generated in which the mouse SP-B cDNA was conditionally expressed under control of exogenous doxycycline in SP-B-/- mice. Doxycycline-regulated expression of SP-B fully corrected lung function in compound SP-B-/- mice and protected mice from respiratory failure at birth. Withdrawal of doxycycline from adult compound SP-B-/- mice resulted in decreased alveolar content of SP-B, causing respiratory failure when SP-B concentration was reduced to