کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5506880 | 1400305 | 2016 | 15 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The effect of H19-miR-29b interaction on bleomycin-induced mouse model of idiopathic pulmonary fibrosis
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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![عکس صفحه اول مقاله: The effect of H19-miR-29b interaction on bleomycin-induced mouse model of idiopathic pulmonary fibrosis The effect of H19-miR-29b interaction on bleomycin-induced mouse model of idiopathic pulmonary fibrosis](/preview/png/5506880.png)
چکیده انگلیسی
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 3â²UTR; miR-29b inhibited COL1A1 expression by directly binding to the 3â²UTR. 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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 479, Issue 3, 21 October 2016, Pages 417-423
Journal: Biochemical and Biophysical Research Communications - Volume 479, Issue 3, 21 October 2016, Pages 417-423
نویسندگان
Yongjun Tang, Ruoxi He, Jian An, Pengbo Deng, Li Huang, Wei Yang,