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. https://doi.org/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. (2017). miR-30a as Potential Therapeutic by Targeting TET1 through Regulation of the Hydroxymethlation of Drp-1 Promoter in IPF. Preprints. https://doi.org/10.20944/preprints201701.0074.v1
Zhang, S., Changjun Lv and Xiaodong Song. 2017 "miR-30a as Potential Therapeutic by Targeting TET1 through Regulation of the Hydroxymethlation of Drp-1 Promoter in IPF" Preprints. https://doi.org/10.20944/preprints201701.0074.v1
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.
Biology and Life Sciences, Biochemistry and Molecular Biology
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