The effect of H19-miR-29b interaction on bleomycin-induced mouse model of idiopathic pulmonary fibrosis

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• 作者：Yongjun Tang ; ^{tyj7736@163.com" class="auth_mail" title="E-mail the corresponding author} ; Ruoxi He ; Jian An ; Pengbo Deng ; Li Huang ; Wei Yang
• 关键词：H19 ; miR-29b ; Bleomycin ; Idiopathic pulmonary fibrosis ; COL1A1 ; Acta2
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2016
• 出版时间：21 October 2016
• 年：2016
• 卷：479
• 期：3
• 页码：417-423
• 全文大小：1404 K

文摘

Pulmonary fibrosis, characterized by the destruction of lung tissue architecture and the formation of fibrous foci, currently has no satisfactory treatment. Emodin is a component of Chinese herb that has been reported to be medicable on pancreatic fibrosis and liver fibrosis. However, its role in pulmonary fibrosis has not been reported yet. In the present study, we investigated the hypothesis that H19 play a promotive role in bleomycin-induced epithelial-mesenchymal transition of alveolar epithelial cell, and H19 exerts its effect through miR-29b regulation. H19 expression was positively correlated with COL1A1 and Acta2 expression; H19 knockdown inhibited COL1A1 and Acta2 expression. Moreover, H19 interacted with miR-29b through directly binding to the 3′UTR; miR-29b inhibited COL1A1 expression by directly binding to the 3′UTR. In conclusion, we revealed the promotive effect of H19 on BLM-induced IPF, and demonstrated the mechanism by which H19/miR-29b interaction exerts its effect on regulating pulmonary fibrosis. The present study provided a potential therapy to treat IPF.