Preprint Article Version 1 This version not peer reviewed

miR-30a as Potential Therapeutic by Targeting TET1 through Regulation of the Hydroxymethlation of Drp-1 Promoter in IPF

These authors contributed equally to this work.
Version 1 : Received: 14 January 2017 / Approved: 16 January 2017 / Online: 16 January 2017 (04:44:44 CET)

How to cite: Zhang, S.; Liu, H.; Liu, Y.; Zhang, J.; Li, H.; Liu, W.; Cao, G.; Xu, P.; Zhang, J.; Lv, C.; Song, X. miR-30a as Potential Therapeutic by Targeting TET1 through Regulation of the Hydroxymethlation of Drp-1 Promoter in IPF. Preprints 2017, 2017010074 (doi: 10.20944/preprints201701.0074.v1). Zhang, S.; Liu, H.; Liu, Y.; Zhang, J.; Li, H.; Liu, W.; Cao, G.; Xu, P.; Zhang, J.; Lv, C.; Song, X. miR-30a as Potential Therapeutic by Targeting TET1 through Regulation of the Hydroxymethlation of Drp-1 Promoter in IPF. Preprints 2017, 2017010074 (doi: 10.20944/preprints201701.0074.v1).

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 the regulation of idiopathic pulmonary fibrosis (IPF) 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 protein-1 (Drp-1). However, the regulatory mechanism between miR-30a and Drp-1 has yet to be investigated. In addition, 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 system assay were used to identify the target gene of miR-30a, and cell transfection was used to confirm this relationship. Ten-eleven translocation 1 (TET1) was validated as a direct target of miR-30a, and the transfection of miR-30a mimic/inhibitor significantly reduced/increased the expression of TET1 protein. Further experiment verified that the interference on TET1(siRNA) could inhibit the hydroxymethlation of the Drp-1 promoter. 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 the TET1 expression by base pairing with complementary sites in the 3′ untranslated region to regulate the hydroxymethlation of the Drp-1 promoter. Furthermore, miR-30a could act as a potential therapeutic target for IPF.

Subject Areas

idiopathic pulmonary fibrosis; miR-30a; TET1; Drp-1

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