Reproduction Axis, Perinatal and Child Health, Room T-1-49, CHUQ Research Center, Québec City, Québec, Canada.
Early Hum Dev. 2010 Sep;86(9):529-34. doi: 10.1016/j.earlhumdev.2010.06.013. Epub 2010 Aug 2.
Co-expression of four apolipoproteins with a sex difference was observed in the mouse developing lung with an increase during the day of the surge of surfactant synthesis and a causal relationship was proposed.
To determine whether these apolipoproteins and lipoprotein lipase (LPL) are expressed in the human fetal lung. To compare the distribution patterns of apoC-II and LPL proteins at different developmental ages.
Real-time PCR with RNA samples and immunohistochemistry with tissues from lungs of fetuses deceased between 19 and 40 weeks' pregnancy.
Elevated apolipoprotein A-I (apoA-I), apoA-II, apoC-II, and apoH expression was observed only during a short gestation time window from 32 to 35 weeks' gestation. LPL was expressed at relatively constant levels over gestation time. The gene encoding for the essential co-factor of LPL, apoC-II, was expressed at similar levels than LPL gene only during the 32-35 week gestation window. ApoC-II and LPL protein distribution vary according to gestation time, with obvious co-localization in capillaries at 32 weeks' gestation, but not in samples collected at 22-24 weeks' gestation.
ApoA-I, apoA-II, apoC-II, and apoH genes are expressed with a human-specific narrow peak of elevated expression in late gestation. Specific and developmental time-dependent distribution profiles were observed for apoC-II and LPL proteins. The 32-35 weeks' gestation window, where high levels of expression of apolipoproteins and co-localization of apoC-II and LPL protein were observed, correlates with the reported decrease in the incidence and severity of respiratory distress syndrome (RDS) consequently to the surge of surfactant synthesis.
在小鼠发育中的肺中观察到四种载脂蛋白与性别差异共同表达，并且在表面活性剂合成激增的白天增加，并提出了因果关系。
确定这些载脂蛋白和脂蛋白脂肪酶 (LPL) 是否在人胎儿肺中表达。比较不同发育年龄时 apoC-II 和 LPL 蛋白的分布模式。
使用来自妊娠 19 至 40 周期间死亡的胎儿肺组织的 RNA 样本进行实时 PCR 和免疫组织化学。
仅在妊娠 32 至 35 周的短妊娠时间窗口观察到载脂蛋白 A-I (apoA-I)、apoA-II、apoC-II 和 apoH 的表达升高。LPL 在整个妊娠期间以相对恒定的水平表达。LPL 的必需辅因子 apoC-II 的编码基因仅在 32-35 周妊娠窗口与 LPL 基因表达水平相似。apoC-II 和 LPL 蛋白的分布根据妊娠时间而变化，在 32 周妊娠时在毛细血管中有明显的共定位，但在 22-24 周妊娠时采集的样本中则没有。
apoA-I、apoA-II、apoC-II 和 apoH 基因在妊娠晚期以人类特异性的高表达高峰表达。观察到 apoC-II 和 LPL 蛋白的特异性和发育时间依赖性分布特征。观察到高水平表达的载脂蛋白和 apoC-II 和 LPL 蛋白的共定位的 32-35 周妊娠窗口与报道的表面活性剂合成激增导致呼吸窘迫综合征 (RDS) 的发生率和严重程度降低相关。
