miR-217/Mafb Axis Involve in High Glucose-Induced beta-TC-tet Cell Damage Via Regulating NF-kappa B Signaling Pathway

摘要

We attempt to explore the role of miR-217 during the process of type 2 diabetes mellitus (T2DM). Mouse beta-TC-tet was dealt with 16.7 mM glucose (HG) to imitate the cells in T2DM. Cell proliferation and apoptosis were determined by cell counting kit-8 and flow cytometry. The correlation between miR-217 and Mafb was predicted with biological software and confirmed by dual lucifierase assay. Western blot was applied to detect protein expression. The data from GEO database exhibited that miR-217 was upregulated in T2DM patients. HG treatment upregulated the expression of miR-217, inhibited the proliferation, and promoted the apoptosis and inflammation of beta-TC-tet cell. Depletion of miR-217 alleviated the damage of beta-TC-tet cell caused by HG. Mafb was affirmed as a target of miR-217 and was negatively modulated by miR-217. Knockdown of Mafb attenuated the alleviation of miR-217 inhibitor on beta-TC-tet cell damage. The expression of key proteins in NF-kappa B signaling pathway was upregulated by HG, and this upregulation tendency was inhibited by miR-217 inhibitor. Moreover, silencing Mafb could alleviate the inhibition of miR-217 inhibitor on these proteins. Our findings insinuated that inhibition of miR-217 could relieve beta-TC-tet damage induced by HG through regulating Mafb and NF-kappa B signaling.