Abstract
Objective To explore the influence and mechanism of cytokines and protein expression of alveolar epithelial type (ACE) II cells in Bama minipigs' right-thorax with a single 15 Gy dose irradiation. Methods All minipigs received either right thoracic irradiation or sham-irradiation under anesthesia. At 4, 8, 12 and 24 week post-irradiation, 5 minipigs respective and random from irradiarion groups and control group were sacrificed to remove the lungs. The protein expression of surfactant associated protein (SP)-A, transforming growth factor (TGF)-β1, Vimentin and E-cadherin were detected by Western blot. The protein expression of α-smooth muscle actin (SMA) was detected by immunohistochemistry. The co-localization of SP-A and α-SMA was visualized by double immunofluorescence staining. Results At 4, 8, 12 and 24 week post-irradiation, a significant increase in the protein expression of α-SMA, TGF-β1 and Vimentin were observed in irradiated lung compared to sham-irradiated controls(α-SMA: t=2.46-3.26, P<0.05; TGF-β1: t=2.96-3.52, P<0.05; Vimentin: t=3.24-5.05, P<0.05). By contrast, the protein expression of SP-A and E-cadherin in irradiation group was lower than it in control group(SP-A: t=3.62-4.65, P<0.05; E-cadherin: t=2.53-4.15, P<0.05). Moreover, at 8 week after irradiation, under confocal laser scanning microscope, the co-localization of SP-A and α-SMA was observed in irradiated alveolar epithelium cells, and it was not observed in sham-irradiated controls. Conclusions These data demonstrate that E-cadherin, SP-A and TGF-β1 may act as sensitive predictors of radiation-induced lung injury(RILI). Irradiation may lead to ACEⅡ cells achieving a mesenchymal phenotype, namely, epithelial to mesenchymal cells transition occurs, and ACEⅡ cells play the important part in the development of RILI by epithelial-mesenchymal transition. Key words: Radiotherapy; Minipigs; Alveolar epithelial type Ⅱ cells; Epithelial-mesenchymal transition
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