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. Preprints2017, 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).
Cite as:
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. Preprints2017, 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.
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Songzi Zhang
†
,