miR-30a as Potential Therapeutics by Targeting TET1 through Regulation of Drp-1 Promoter Hydroxymethylation in Idiopathic Pulmonary Fibrosis
作者： Songzi Zhang , Huizhu Liu , Yuxia Liu , Jie Zhang , Hongbo Li
DOI: 10.3390/IJMS18030633
关键词:
摘要: Several recent studies have indicated that miR-30a plays critical roles in various biological processes and diseases. However, the mechanism of participation idiopathic pulmonary fibrosis (IPF) regulation is ambiguous. Our previous study demonstrated may function as a novel therapeutic target for lung by blocking mitochondrial fission, which dependent on dynamin-related protein1 (Drp-1). regulatory between Drp-1 yet to be investigated. Additionally, whether can act potential has not been verified vivo. In this study, expression IPF patients was evaluated. Computational analysis dual-luciferase reporter assay system were used identify gene miR-30a, cell transfection utilized confirm relationship. Ten–eleven translocation 1 (TET1) validated direct mimic inhibitor significantly reduced increased TET1 protein expression, respectively. Further experimentation siRNA interference could inhibit promoter hydroxymethylation. Finally, agomir designed applied validate effect through base pairing with complementary sites 3′untranslated region regulate Furthermore, IPF.
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