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首页> 外文期刊>American Journal of Physiology >TGF-alpha perturbs surfactant homeostasis in vivo.
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TGF-alpha perturbs surfactant homeostasis in vivo.

机译：TGF-α在体内干扰表面活性剂的体内稳态。

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摘要

To determine potential relationships between transforming growth factor (TGF)-alpha and surfactant homeostasis, the metabolism, function, and composition of surfactant phospholipid and proteins were assessed in transgenic mice in which TGF-alpha was expressed in respiratory epithelial cells. Secretion of saturated phosphatidylcholine was decreased 40-60% by expression of TGF-alpha. Although SP-A, SP-B, and SP-C mRNA levels were unchanged by expression of TGF-alpha, SP-A and SP-B content in bronchoalveolar lavage fluid was decreased. The minimum surface tension of surfactant isolated from the transgenic mice was significantly increased. Incubation of cultured normal mice type II cells with TGF-alpha in vitro did not change secretion of surfactant phosphatidylcholine and SP-B, indicating that TGF-alpha does not directly influence surfactant secretion. Expression of a dominant negative (mutant) EGF receptor in the respiratory epithelium blocked the TGF-alpha-induced changes in lung morphology and surfactant secretion, indicating that EGF receptor signaling in distal epithelial cells was required for TGF-alpha effects on surfactant homeostasis. Because many epithelial cells were embedded in fibrotic lesions caused by TGF-alpha, changes in surfactant homeostasis may at least in part be influenced by tissue remodeling that results in decreased surfactant secretion. The number of nonembedded type II cells was decreased 30% when TGF-alpha was expressed during development and was increased threefold by TGF-alpha expression in adulthood, suggesting possible alteration of type II cells on surfactant metabolism in the adult lung. Abnormalities in surfactant function and decreased surfactant level in the airways may contribute to the pathophysiology induced by TGF-alpha in both the developing and adult lung.
机译：为了确定转化生长因子（TGF）-α与表面活性剂稳态之间的潜在关系，在其中呼吸道上皮细胞中表达TGF-α的转基因小鼠中评估了表面活性剂磷脂和蛋白质的代谢，功能和组成。通过表达TGF-α，饱和磷脂酰胆碱的分泌减少了40-60％。尽管通过TGF-α的表达，SP-A，SP-B和SP-C mRNA水平未改变，但支气管肺泡灌洗液中SP-A和SP-B含量降低。从转基因小鼠分离的表面活性剂的最小表面张力显着增加。用TGF-α在培养的正常II型小鼠细胞中孵育不会改变表面活性剂磷脂酰胆碱和SP-B的分泌，表明TGF-α不会直接影响表面活性剂的分泌。呼吸道上皮细胞中显性负（突变）EGF受体的表达阻断了TGF-α诱导的肺形态和表面活性剂分泌的变化，这表明TGF-α对表面活性剂稳态的影响需要远端上皮细胞中的EGF受体信号传导。由于TGF-α引起的纤维化病变中嵌有许多上皮细胞，因此表面活性剂稳态的变化可能至少部分受到组织重塑的影响，从而导致表面活性剂分泌减少。在发育过程中表达TGF-α时，未包埋的II型细胞数量减少了30％，在成年期由于TGF-α表达而增加了三倍，表明成人肺中表面活性剂代谢可能改变了II型细胞。表面活性剂功能异常和气道表面活性剂水平降低可能与TGF-α在发育中和成年肺中引起的病理生理有关。

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