دورية أكاديمية

In vivo therapeutic success of MicroRNA-155 antagomir in a mouse model of pulmonary fibrosis induced by bleomycin

التفاصيل البيبلوغرافية
العنوان: In vivo therapeutic success of MicroRNA-155 antagomir in a mouse model of pulmonary fibrosis induced by bleomycin
المؤلفون: Xiaoyuan Sun, Yu Kang, Shan Xue, Jing Zou, Jiabo Xu, Daoqiang Tang, Hui Qin
المصدر: The Korean Journal of Internal Medicine, Vol 36, Iss Suppl 1, Pp S160-S169 (2021)
بيانات النشر: The Korean Association of Internal Medicine, 2021.
سنة النشر: 2021
المجموعة: LCC:Medicine
مصطلحات موضوعية: pulmonary fibrosis, microrna-155, antagomir, bleomycin, Medicine
الوصف: Background/Aims MicroRNAs (miRNAs) play critical regulatory roles in the pathogenesis of pulmonary fibrosis. The aim of this study was to explore whether miRNA antagomirs could serve as potential therapeutic agents in interstitial lung diseases. Methods A mouse model of pulmonary fibrosis was established by intratracheal injection of bleomycin (BLM). Using microarray analysis, up-regulated miRNAs were identified during the development of pulmonary fibrosis. miR-155 was chosen as the candidate miRNA. Fifteen mice were then randomized into the following three groups: BLM + antagomiR-155 group, treated with BLM plus intravenously injected with antagomiR-155; BLM group, treated with intratracheal BLM plus phosphate-buffered saline (PBS); and a control group, treated with PBS only. Lung tissues were collected for histopathological analysis, hydroxyproline measurement, and Western blotting. Enzyme-linked immunosorbent assays were used for the measurement of cytokines associated with pulmonary fibrosis. Results Histological changes and hydroxyproline levels induced by BLM were significantly inhibited by antagomiR-155. The levels of interleukin 4 (IL-4) and transforming growth factor-β (TGF-β) expression were increased after BLM treatment. However, miR-155 silencing decreased the expression of IL-4, TGF-β, and interferon-γ. TGF-β-activated kinase 1/mitogen-activated protein kinase kinase kinase 7 (MAP3K7)-binding protein 2 (TAB2) of the mitogen-activated protein kinase (MAPK) signaling pathway, was activated by BLM and inhibited by in vivo silencing of miR-155 via antagomiR-155. Conclusions In vivo treatment with antagomiR-155 alleviated the pathological changes induced by BLM and may be a promising therapeutic strategy for pulmonary fibrosis.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1226-3303
2005-6648
Relation: http://www.kjim.org/upload/pdf/kjim-2019-098.pdf; https://doaj.org/toc/1226-3303; https://doaj.org/toc/2005-6648
DOI: 10.3904/kjim.2019.098
URL الوصول: https://doaj.org/article/a8a230567f2f4797a3a789ae72fc54ed
رقم الأكسشن: edsdoj.8a230567f2f4797a3a789ae72fc54ed
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:12263303
20056648
DOI:10.3904/kjim.2019.098