Coordination of growth and differentiation in the fetal lung.
Coordination of growth and differentiation in the fetal lung.
复制标题
胎肺生长和分化的协调。
DOI：
10.1016/0014-4827(90)90281-e
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发表时间：
1990
影响因子：
3.7
通讯作者：
Torday,JS
中科院分区：
文献类型：
--
作者：
Nielsen,HC;Kirk,WO;Sweezey,N;Torday,JS
男性胎肺在妊娠期开始合成表面活性剂的时间晚于女性。这种延迟似乎是由雄激素引起的。我们假设雄性胎儿肺分化延迟是由于雄激素引起的生长阶段延长的结果。我们观察到，相对于 DNA 合成，体内胎儿肺蛋白质合成在雌性胎儿肺的妊娠早期达到峰值，并且该事件与分化的开始同步。怀孕期间对怀孕的大鼠进行双氢睾酮（DHT）治疗，并测量胎肺生长参数。 DHT 处理显着提高了肺湿重、干重以及 DNA 和蛋白质浓度。从 DHT 治疗胎儿的肺部分离出 II 型细胞和成纤维细胞。回收的总细胞数增加30%；回收的II型细胞数量增加了87%；恢复的成纤维细胞数量增加了42%。与来自对照肺的细胞相比，回收的II型细胞表现出[3H]胸苷掺入DNA的增加以及放射性标记的蛋白质与放射性标记的DNA的比率降低。进一步的研究是在体外使用从未经处理的胎鼠肺中分离出的成纤维细胞和 II 型细胞进行的。培养过程中用 DHT 处理成纤维细胞导致胸苷掺入 DNA 的量增加。这种效应并不能被皮质醇同时治疗所阻断，皮质醇通常会导致 DNA 合成减少并诱导成纤维细胞分化。在培养物中用 DHT 处理 II 型细胞导致细胞数量呈剂量依赖性增加，但二饱和磷脂酰胆碱的合成减少。这些研究为胎儿肺生长控制和分化控制之间的相互关系提供了更直接的证据。 DHT 是一种延迟分化表达开始的信号，也能诱导生长。我们得出的结论是，胎儿肺的生长和分化的控制是相互关联的。
The male fetal lung begins to synthesize surfactant later in gestation than the female. This delay appears to be caused by androgens. We hypothesized that male fetal lung differentiation is delayed as a consequence of an extended phase of growth which is elicited by androgens. We observed thatin vivofetal lung protein synthesis relative to DNA synthesis peaked earlier in gestation in the female fetal lung and that this event was synchronous with the onset of differentiation. Pregnant rats were treated with dihydrotestosterone (DHT) during pregnancy, and fetal lung growth parameters were measured. Lung wet weight, dry weight, and DNA and protein concentrations were significantly elevated by DHT treatment. Type II cells and fibroblasts were isolated from lungs of DHT-treated fetuses. The number of total cells recovered was increased by 30%; the number of type II cells recovered was increased by 87%; and the number of fibroblasts recovered was increased by 42%. The type II cells which were recovered exhibited increased incorporation of [3H]thymidine into DNA and a reduced ratio of radiolabeled protein to radiolabeled DNA compared to that of cells from control lungs. Further studies were donein vitrowith fibroblasts and type II cells isolated from untreated fetal rat lungs. Treatment of the fibroblasts with DHT during culture caused an increase in thymidine incorporation into DNA. This effect was not blocked by simultaneous treatment with cortisol, which normally causes reduced DNA synthesis and induces fibroblast differentiation. Treatment of the type II cells with DHT in culture caused a dose-dependent increase in cell number but a decrease in synthesis of disaturated phosphatidylcholine. These studies provide more direct evidence of the interrelationships between the control of growth and the control of differentiation in the fetal lung. DHT, a signal which delays the onset of expression of differentiation, also induces growth. We conclude that the controls of growth and of differentiation of the fetal lung are reciprocally linked.