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23. Glycogen synthase kinase‐3β promotes radiation‐induced lung fibrosis by regulating β‐catenin/lin28 signaling network to determine type II alveolar stem cell transdifferentiation state

Author

Zhang, Tingting, primary, Zhou, Jianwei, additional, Yue, Haodi, additional, Du, Chunyan, additional, Xiao, Ziting, additional, Zhao, Wendi, additional, Li, Na, additional, Wang, Xiangdong, additional, Liu, Xiaozhuan, additional, Li, Yanjun, additional, Geng, Xiwen, additional, Zhang, Yuwei, additional, Li, Li, additional, and Tian, Jian, additional

Published
2020
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24. β-Catenin/Lin28/let-7 regulatory network determines type II alveolar epithelial stem cell differentiation phenotypes following thoracic irradiation.

Author

Liu, Xiaozhuan, Zhang, Tingting, Zhou, Jianwei, Xiao, Ziting, Li, Yanjun, Zhang, Yuwei, Yue, Haodi, Li, Zhitao, and Tian, Jian

Subjects
CELL differentiation, STEM cells
Abstract

The contribution of type II alveolar epithelial stem cells (AEC II) to radiation-induced lung fibrosis (RILF) is largely unknown. Cell differentiation phenotypes are determined by the balance between Lin28 and lethal-7 microRNA (let-7 miRNA). Lin28 is activated by β-catenin. The aim of this study was to track AEC II phenotypes at different phases of injury following thoracic irradiation and examine the expression of β-catenin, Lin28 and let-7 to identify their role in AEC II differentiation. Results showed that coexpression of prosurfactant protein C (proSP-C, an AEC II biomarker) and HOPX (homeobox only protein X, an AEC I biomarker) or vimentin (a differentiation marker) was detected in AEC II post-irradiation. The protein expression levels of HOPX and proSP-C were significantly downregulated, but vimentin was significantly upregulated following irradiation. The expression of E-cadherin, which prevents β-catenin from translocating to the nucleus, was downregulated, and the expression of β-catenin and Lin28 was upregulated after irradiation (P  < 0.05 to P  < 0.001). Four let-7 miRNA members (a, b, c and d) were upregulated in irradiated lungs (P  < 0.05 to P  < 0.001), but let-7d was significantly downregulated at 5 and 6 months (P  < 0.001). The ratios of Lin28 to four let-7 members were low during the early phase of injury and were slightly higher after 2 months. Intriguingly, the Lin28/let-7d ratio was strikingly increased after 4 months. We concluded that β-catenin contributed to RILF by promoting Lin28 expression, which increased the number of AEC II and the transcription of profibrotic molecules. In this study, the downregulation of let-7d miRNA by Lin28 resulted in the inability of AEC II to differentiate into type I alveolar epithelial cells (AEC I). [ABSTRACT FROM AUTHOR]

Published
2021
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