Gao Rui-wei, Kong Xiang-yong, Zhu Xiao-xi, Zhu Guo-qing, Ma Jin-shuai, Liu Xiu-xiang
Binzhou Medical University, Yantai, 264000, Shandong, China.
In Vitro Cell Dev Biol Anim. 2015 May;51(5):479-87. doi: 10.1007/s11626-014-9850-2. Epub 2014 Dec 17.
Retinoic acid (RA) plays an important role in lung development and maturation. Many stimuli can induce alveolar epithelial cell damage which will result in the injury of lung parenchyma. The aim of this study was to observe the effect of RA on the proliferation and differentiation of primary fetal alveolar epithelial type II cells (fAECIIs). Primary fAECIIs were isolated from fetal rats at 19 d of gestation and purified by a differential centrifugation and adhesion method. The cells were randomly divided into control (dimethyl sulfoxide, DMSO) and RA groups. Cell proliferation, viability, apoptosis, cycle, and expression of target protein were examined at 24, 48, and 72 h. We found that the proliferation and viability of cells in the RA-exposed group significantly increased compared with the DMSO control group. The proportion (%) of cells in the G2 and S phases in the RA group was significantly higher than that in control group cells. The proportion (%) of both early apoptotic cells and late apoptotic cells decreased significantly in cells exposed to RA compared with cells exposed to DMSO. RA significantly enhanced the expression of aquaporin 5 (AQP5). The expression level of pulmonary surfactant C (SPC) was elevated after cells were exposed to RA for 24 and 72 h but was inhibited when cells were exposed to RA for 48 h. These results suggest that RA promotes fAECII proliferation by improving cell viability, promoting S phase entry and inhibiting apoptosis and RA promotes fAECIIs differentiation to alveolar epithelial type I cells (AECIs).
视黄酸（RA）在肺的发育和成熟过程中发挥着重要作用。许多刺激因素可诱导肺泡上皮细胞损伤，进而导致肺实质损伤。本研究旨在观察RA对原代胎儿肺泡II型上皮细胞（fAECIIs）增殖和分化的影响。从妊娠19天的胎鼠中分离出原代fAECIIs，并通过差速离心和贴壁法进行纯化。将细胞随机分为对照组（二甲基亚砜，DMSO）和RA组。在24、48和72小时检测细胞增殖、活力、凋亡、周期及靶蛋白表达。我们发现，与DMSO对照组相比，RA处理组细胞的增殖和活力显著增加。RA组细胞中G2期和S期的细胞比例（%）显著高于对照组细胞。与DMSO处理的细胞相比，RA处理的细胞中早期凋亡细胞和晚期凋亡细胞的比例（%）均显著降低。RA显著增强了水通道蛋白5（AQP5）的表达。细胞暴露于RA 24和72小时后，肺表面活性物质C（SPC）的表达水平升高，但细胞暴露于RA 48小时时，SPC表达受到抑制。这些结果表明，RA通过提高细胞活力、促进细胞进入S期和抑制凋亡来促进fAECII增殖，并且RA促进fAECIIs向肺泡I型上皮细胞（AECIs）分化。
