Effect of 17β‐Estradiol on Endothelial Cell Expression of Inflammation‐Related miRNAs

Abstract

MicroRNAs (miRs) are short single stranded noncoding RNAs that are involved in the regulation of a number of physiological and pathological processes. miRs down regulate target gene expression post‐transcriptionally by degrading messenger RNA and/or by blocking translation. It is now recognized that miRs play a key role in regulating inflammatory processes underlying cardiovascular disease (CVD). For example, altered expression of specific miRs, such as miR‐126, miR‐146a, miR‐150 and miR‐181b have been linked with heightened vascular inflammation, atherosclerosis and CVD risk. It is well established that 17β‐estradiol is anti‐inflammatory and vasculo‐protective. Indeed, 17β‐estradiol‐mediated reductions in vascular inflammation have been linked with reduced pathogenesis of CVD. However, the mechanisms by which 17β‐estradiol influences vascular inflammation are not fully understood. Accordingly, the aim of this study was to determine the effects of 17β‐estradiol on endothelial cell expression of miR‐126, miR‐146a, miR‐150 and miR‐181b. Cultured human umbilical vein endothelial cells (HUVECs) were plated at a density of 5.0×105 cells/condition. Cells were treated with media alone or media containing 17β‐estradiol (100 nM) for 48 h. To determine miR expression, RNA was extracted from 1.0×105 cells and quantified using RT‐PCR. Cellular expression was normalized to RNU6 and calculated as fold change in ΔΔCt from control (N=4, experimental units). Cellular expression of miR‐126 (2.40±0.56 fold), miR‐146a (2.40±0.58 fold), miR‐150 (2.01±0.36 fold) and miR‐181b (2.47±0.56 fold) was significantly increased (240%, 240%, 200% and 250% respectively) in response to 17β‐estradiol treatment compared with control. These data indicate that 17β‐estradiol beneficially affects cellular expression of inflammation‐associated miRs. Higher cellular expression of miR‐126, miR‐146a, miR‐150 and miR‐181b is associated with reduced vascular inflammation by targeting nuclear factor κB (NFκB) activity. The alteration of the cellular expression of these miRs may play a role in the anti‐inflammatory and vasculo‐protective effects of 17β‐estradiol.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.