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Int. J. Mol. Sci. 2017, 18(3), 633; doi:10.3390/ijms18030633

miR-30a as Potential Therapeutics by Targeting TET1 through Regulation of Drp-1 Promoter Hydroxymethylation in Idiopathic Pulmonary Fibrosis

1
Department of Cellular and Genetic Medicine, School of Pharmaceutical Sciences, Binzhou Medical University, Yantai 264003, China
2
Department of Clinical Pharmacology, School of Pharmaceutical Sciences, Taishan Medical University, Taishan 271016, China
3
Department of Respiratory Medicine, Affiliated Hospital to Binzhou Medical University, Binzhou 256602, China
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Academic Editor: Constantinos Stathopoulos
Received: 16 January 2017 / Revised: 3 March 2017 / Accepted: 7 March 2017 / Published: 15 March 2017
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Abstract

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

Zhang, S.; Liu, H.; Liu, Y.; Zhang, J.; Li, H.; Liu, W.; Cao, G.; Xv, P.; Zhang, J.; Lv, C.; Song, X. miR-30a as Potential Therapeutics by Targeting TET1 through Regulation of Drp-1 Promoter Hydroxymethylation in Idiopathic Pulmonary Fibrosis. Int. J. Mol. Sci. 2017, 18, 633.

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