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  • Title: Inhibition of EZH2 attenuates coronary heart disease by interacting with microRNA-22 to regulate the TXNIP/nuclear factor-κB pathway.
    Author: Liu Y, Dai C, Lei Y, Wu W, Liu W.
    Journal: Exp Physiol; 2020 Dec; 105(12):2038-2050. PubMed ID: 33026112.
    Abstract:
    NEW FINDINGS: What is the central question of this study? The relevance of microRNA-22 (miR-22) has been indicated in coronary heart disease (CHD). How does it exert a protective role in CHD? What is the main finding and its importance? EZH2 inhibited transcription of the miR-22 promoter, thus modulating cell proliferation in human umbilical vein endothelial cells and vascular smooth muscle cells to induce CHD. ABSTRACT: MicroRNA-22 (miR-22) was indicated to modulate cell proliferation in human umbilical vein endothelial cells (HUVECs) under exposure to environmental toxicants. In the present study, we investigated the involvement of miR-22 in the mediation of HUVEC and vascular smooth muscle cell (VSMC) function, hence in the development of coronary heart disease (CHD). miR-22 expression was reduced in serum of CHD patients. Restoration of miR-22 decreased the proliferation, migration and invasion of VSMCs and increased apoptotic cells and inflammatory factors. In contrast, upregulation of miR-22 led to opposite trends in HUVECs. Chromatin immunoprecipitation and dual-luciferase assays validated that enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) inhibited transcription of miR-22 promoter. EZH2, overexpressed in serum from CHD patients, diminished VSMC apoptosis, but facilitated HUVEC apoptosis. Luciferase reporter assays confirmed that thioredoxin-interacting protein (TXNIP) was a new direct target of miR-22. Overexpression of TXNIP blocked the function of miR-22 in HUVECs and VSMCs. Taken together, these findings will shed light on the role and mechanism of EZH2 in viability, migration, invasion and apoptosis via the miR-22/TXNIP axis in VSMCs and HUVECs, which might provide new insights into the treatment of CHD.
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