Department of Pediatrics, the Affiliated Hospital of Jiangsu University, Zhenjiang, China.
In Vitro Cell Dev Biol Anim. 2011 Jan;47(1):64-72. doi: 10.1007/s11626-010-9360-9. Epub 2010 Nov 17.
Hyperoxia exposure is a significant risk factor for the impaired alveolarization characteristic of bronchopulmonary dysplasia. Type II alveolar epithelial cells (AECIIs) may serve as "alveolar stem cells" to transdifferentiate into type I alveolar epithelial cells (AECIs). Here, we show that hyperoxia is capable of inducing transdifferentiation of AECIIs in premature rats in vitro. Hyperoxia-induced transdifferentiation was characterized by typical morphological changes, inhibition of cellular proliferation, decline in expression rate of Ki67, accumulation of cells in the G(1) phase of the cell cycle, increased expression of AECI-specific protein aquaporin 5, and decreased expression of AECII-associated protein surfactant protein C. These results suggest that hyperoxia may induce transdifferentiation of AECIIs into AECIs and the transdifferentiation may be responsible for repairing early lung injury.
高氧暴露是导致支气管肺发育不良肺泡化受损的一个重要危险因素。II 型肺泡上皮细胞(AECII)可能作为“肺泡干细胞”向 I 型肺泡上皮细胞(AECI)转分化。在这里,我们证明高氧能够在体外诱导早产大鼠 AECII 的转分化。高氧诱导的转分化表现为典型的形态学变化,细胞增殖受到抑制,Ki67 表达率下降,细胞周期 G1 期积累,AECI 特异性蛋白水通道蛋白 5 表达增加,AECII 相关蛋白表面活性蛋白 C 表达减少。这些结果表明,高氧可能诱导 AECII 向 AECI 转分化,这种转分化可能是修复早期肺损伤的原因。