The Impact of MiR-33a-5p Inhibition in Pro-Inflammatory Endothelial Cells

Evidence suggests cholesterol accumulation in pro-inflammatory endothelial cells (EC) contributes to triggering atherogenesis and driving atherosclerosis progression. Therefore, inhibiting miR-33a-5p within inflamed endothelium may prevent treat by enhancing apoAI-mediated efflux upregulating ABCA1. However, it is not entirely elucidated whether inhibition of EC capable increasing ABCA1-dependent efflux. In our study, we initially transfected LPS-challenged, immortalized mouse aortic (iMAEC) with either pAntimiR33a5p plasmid DNA or the control plasmid, pScr. We detected significant increases both ABCA1 protein expression iMAEC when compared subsequently used polymersomes targeting deliver pScr cultured showed that were selective iMAEC. Moreover, exposed LPS-challenged these polymersomes, observed a decrease incubated containing pAntimR33a5p versus also non-significant Based on results, exhibits atheroprotective effects, so precisely delivering anti-miR-33a-5p promising anti-atherogenic strategy.