Hong-Yan Lu1, Li-Wen Chang, Hong Wang, Wen-Bin Li, Hua Wang. 1. Department of Pediatrics, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. lhy5154@163.com
Abstract
AIM: To investigate the effect of hyperoxia on the transdifferentiation of type II alveolar epithelial cells (AECII) in premature delivery rats. METHODS: AECII from fetal rat lung were cultured primarily to establish a model of cells damaged by hyperoxia. The morphological changes of the cells were observed by inverted phase contrast microscope and transmission electron microscope. AECII-specific surfactant protein C (SP-C) and AECI-specific aquaporin 5 (AQP5) were detected by immunocytochemical staining. The expression levels of SP-C, AQP5 mRNAs and their protein were detected by RT-PCR and flow cytometry. RESULTS: With the time of exposure to hyperoxia, primarily cultured AECII spread and flattened, losing lamellar bodies and microvilli. They rapidly lost their characteristics and gained some AECI appearance. With their morphological changes, AECII stopped expressing AECII-specific protein SP-C but began expressing AECI-associated protein AQP5. Compared with exposure to air at the same time in air group for 24, 48 and 72 hours, the expression rate of SP-C mRNA in positive cells and fluorescence index (FI) decreased markedly in 3 groups, but compared with exposure to air for 24 and 48 hours the expression of AQP5 increased significantly in 2 groups. The expression of AQP5 began decreasing and showed no marked difference compared with air group at the same time of for 72 hours. CONCLUSION: The transdifferentiation of AECII induced by hyperoxia may play a key role in the repair of alveolar epithelial cell injury in premature delivery rats.
AIM: To investigate the effect of hyperoxia on the transdifferentiation of type II alveolar epithelial cells (AECII) in premature delivery rats. METHODS: AECII from fetal rat lung were cultured primarily to establish a model of cells damaged by hyperoxia. The morphological changes of the cells were observed by inverted phase contrast microscope and transmission electron microscope. AECII-specific surfactant protein C (SP-C) and AECI-specific aquaporin 5 (AQP5) were detected by immunocytochemical staining. The expression levels of SP-C, AQP5 mRNAs and their protein were detected by RT-PCR and flow cytometry. RESULTS: With the time of exposure to hyperoxia, primarily cultured AECII spread and flattened, losing lamellar bodies and microvilli. They rapidly lost their characteristics and gained some AECI appearance. With their morphological changes, AECII stopped expressing AECII-specific protein SP-C but began expressing AECI-associated protein AQP5. Compared with exposure to air at the same time in air group for 24, 48 and 72 hours, the expression rate of SP-C mRNA in positive cells and fluorescence index (FI) decreased markedly in 3 groups, but compared with exposure to air for 24 and 48 hours the expression of AQP5 increased significantly in 2 groups. The expression of AQP5 began decreasing and showed no marked difference compared with air group at the same time of for 72 hours. CONCLUSION: The transdifferentiation of AECII induced by hyperoxia may play a key role in the repair of alveolar epithelial cell injury in premature delivery rats.