T2DM inhibition of endothelial miR-342-3p facilitates angiogenic dysfunction via repression of FGF11 signaling.

Biochemical and Biophysical Research Communications
Shaoyun ChengYu-Zhong Hua

Abstract

Understanding the function and molecular relevance of distinct miRNAs in endothelial cells (ECs) paves avenues for possible therapeutic intervention by targeting epigenetic mechanisms in vascular endothelial dysfunction, one of the major complications of type 2 diabetes mellitus (T2DM). MiR-342-3p, an obesity-associated miRNA, has recently been shown to be significantly upregulated in human angiosarcoma compared to benign hemangioma, indicating its potential involvement as a proangiogenic factor. Herein, we show that endothelial miR-342-3p expression was significantly compromised in T2DM organisms and this inhibition powerfully blocked vasculogenesis in vivo by repressing endothelial proliferation and migration. From a mechanistic standpoint, miR-342-3p promoted the transactivation of fibroblast growth factor 11 (FGF11) by directly targeting its 3' untranslated regions (3'UTRs). Functionally, overexpression of exogenous FGF11 successfully rescued miR-342-3p deficiency-impaired endothelial proliferation and migration. Thus, perturbation of miR-342-3p/FGF11 cascade by hyperinsulinemia plays a causative role in the induction of vascular dysfunction in T2DM. Overall, the current study underscore an endothelial facet of miR-342-3p, ...Continue Reading

Citations

Nov 22, 2019·The Journal of Obstetrics and Gynaecology Research·Xiuhua HanLili Sun
Mar 5, 2020·Scientific Reports·Hyo Youl MoonJi-Seok Kim
May 3, 2020·Cell Communication and Signaling : CCS·Martyna SochackaMalgorzata Zakrzewska
Jun 20, 2019·International Journal of Molecular Sciences·Celeste CocoMonica Montagnani

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