Background: Angiotensin II (Ang II)-induced damage to endothelial cells (ECs) plays a crucial role in the pathogenesis of atherosclerosis. This study aimed to investigate the role of microRNA-384 (miR-384) in endothelial cell apoptosis. Methods: The expression of five various miRNAs in Ang II-treated human umbilical vein endothelial cells (HUVECs) were detected by qPCR. The Ang II -induced apoptosis of HUVEC5 was determined by flow cytometry, TUNEL staining and western blot. Endoplasmic reticulum (ER) stress markers were detected by western blot analysis. The target gene of miR-384 was determined by bioinformatics analyses. qPCR, western blotting and immunofluorescence were performed to determine the expression level of homocysteine inducible ER protein with ubiquitin like domain 1 (Herpud1). Results: miR-384 expression level was significantly decreased in Ang II-treated HUVECs. Ang II -induced HUVEC apoptosis was accompanied by the occurrence of ER stress. A decreased rate of HUVEC apoptosis and a decreased rate of ER stress were observed following restoration of miR-384 expression. Herpudl expression level was increased in HUVECs treated with Ang II, and miR-384 mimics effectively inhibited Herpudl expression. Mechanistically, miR-384 directly targets the 3'-untranslated region of Herpudl. Furthermore, effects of miR-384 on HUVECs apoptosis and ER stress were at least partly reversed by knockdown of Herpudl expression. Conclusion: The results of the present study collectively indicated that miR-384 expression level was downregulated in Ang II-treated HUVECs and miR-384 overexpression protected HUVECs against Ang II induced apoptosis by negatively regulating Herpudl. These findings point towards new strategies by which apoptosis of ECs can be suppressed. (C) 2017 Elsevier Inc. All rights reserved.