MicroRNAs (miRNAs) are short single stranded RNAs that have gene regulatory functions primarily via binding to complementary mRNA transcripts that are either degraded or translationally inhibited in the process. In endothelial cells, miRNAs have a multitude of functions ranging from the regulation of cell proliferation and angiogenesis to cellular senescence and apoptosis, and also vascular inflammatory processes are critically affected by miRNAs. Furthermore, recent findings indicate that miRNAs encapsulated into microparticles are secreted from endothelial cells to affect adjacent endothelial and smooth muscle cells and more remote cells via circulation, suggesting that endothelium-derived miRNAs have paracrine and endocrine functions. As oxidative stress is important in many vascular diseases such as atherosclerosis, we aim to elucidate the role of miRNAs in antioxidant defense in endothelial cells. Specifically, we have studied the antioxidant response element (ARE) mediated regulation of cytoprotective heme oxygenase-1 (HO-1) gene by the transcriptional repressor Bach1, and have shown that oligonucleotides mimicking miR-155 inhibit Bach1 protein translation, resulting in an increase in HO-1 expression. Moreover, endogenous miR-155 is induced by TNFa via an NF-kB-dependent mechanism with a subsequent increase in HO-1, suggesting indirect regulation of HO-1 by TNFa via ARE. In addition, we have studied how oxidized phospholipid 1-palmitoyl-2-arachidonyl-sn- glycero-3-phosphorylcholine (oxPAPC) formed during oxidation of membrane phospholipids and lipoproteins affects miRNA expression in endothelial cells. Furthermore, the interplay between transcriptional regulation of genes by the antioxidative transcription factor Nrf2 and endothelial miRNAs is discussed.