Peroxisome proliferator-activated receptor gamma and ligands inhibit surfactant protein B gene expression in the lung.
Peroxisome proliferator-activated receptor gamma and ligands inhibit surfactant protein B gene expression in the lung.
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过氧化物酶体增殖物激活受体 γ 和配体抑制肺中表面活性蛋白 B 基因的表达。
DOI：
10.1074/jbc.m304156200
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Du,Hong
中科院分区：
文献类型：
--
作者：
Yang,Li;Yan,Dong;Yan,Cong;Du,Hong
肺无纤毛细支气管上皮细胞(Clara细胞)和肺泡II型(AT II)上皮细胞负责表面活性物质的合成和分泌。这些细胞是高度造脂的，具有很高的脂肪周转率。虽然只有10%的表面活性物质是中性脂，但它们在维持肺表面活性物质的动态平衡方面起着非常重要的作用。许多中性脂质的代谢中间产物作为各种核受体的配体，与靶基因结合，影响基因转录。本报告探讨了中性脂代谢产物15-脱氧-Δ、12，14-前列腺素J_2和9-羟基十八烷酸，以及过氧化体增殖物激活受体γ在表面活性蛋白B基因调控中的作用。这些试剂在转录水平下调呼吸道上皮细胞表面活性蛋白B基因的表达，在细胞系和全肺外植体系统中都是如此。这些研究支持肺表面活性蛋白B动态平衡受肺内中性脂类代谢产物影响的观点。
Pulmonary nonciliated bronchiolar epithelial cells (Clara cells) and alveolar type II (AT II) epithelial cells are responsible for surfactant synthesis and secretion. These cells are highly lipogenic with a high lipid turnover rate. Although only 10% of surfactant lipids are neutral lipids, they play very important roles in maintaining pulmonary surfactant homeostasis. Many metabolic intermediate products of neutral lipids serve as ligands for various nuclear receptors that bind to target genes to influence gene transcription. In this report, the functional role of the neutral lipid metabolites, 15-deoxy-Δ12,14-prostaglandin J2and 9-hydroxyoctadecanoic acids, and peroxisome proliferator-activated receptor γ was evaluated in surfactant protein B gene regulation. These reagents down-regulated surfactant protein B gene expression in respiratory epithelial cells at the transcriptional level in both cell line and whole lung explant systems. The studies support the concept that surfactant protein B homeostasis is influenced by neutral lipid metabolites in the lung.