Changes in gene expression in hyperoxia-induced neonatal lung injury.
Changes in gene expression in hyperoxia-induced neonatal lung injury.
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高氧诱导的新生儿肺损伤中基因表达的变化。
DOI：
10.1152/ajplung.1990.258.2.l107
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Quible,DJ
中科院分区：
文献类型：
--
作者：
Horowitz,S;Shapiro,DL;Finkelstein,JN;Notter,RH;Johnston,CJ;Quible,DJ
暴露在高浓度氧气(高氧)中会导致肺损伤。这种损伤的生化基础尚不清楚，但很可能包括基因表达的变化。高氧诱导的(H-I)cDNA已经被分子克隆(Horowitz等人)。J.Biol.化学。264：7092-7095,1989)。其中一个(H-I-1)编码金属蛋白酶组织抑制因子(TIMP)，它是细胞外基质转换的关键调节蛋白。在这里，我们鉴定了另一个克隆(H-I3)，编码肺表面活性物质载脂蛋白A(SP-A)。新生兔暴露于100%氧气96h后，与TIMP、SP-A和另一H-I基因对应的mRNAs增加。这些研究已经开始探索与新生儿高氧性肺损伤相关的基因表达的具体变化。
Exposure to high concentrations of oxygen (hyperoxia) can result in lung injury. The biochemical basis of this injury is poorly understood, but it is likely to include alterations in gene expression. Hyperoxia-induced (H-I) cDNAs have been molecularly cloned (Horowitz et al. J. Biol. Chem. 264: 7092-7095, 1989) from the lungs of an adult rabbit exposed to toxic levels of oxygen. One of them (H-I 1) was identified as encoding the tissue inhibitor of metalloproteinases (TIMP), a key regulatory protein of extracellular matrix turnover. Here we identify another clone (H-I 3) as encoding pulmonary surfactant apoprotein A (SP-A). We also show that in neonatal rabbits exposed to 100% oxygen for 96 h, the mRNAs corresponding to TIMP, SP-A, and another H-I gene are increased. These studies have begun to explore specific changes in gene expression associated with neonatal hyperoxic lung injury.