Details

Autor(en) / Beteiligte

• Zhang, Ping
• Luo, Jianfang
• Wu, Tianlong
• Wang, Xuan
• Yang, Fan
• Yu, Yanhong
• Lu, Lihe
• Yu, Huimin

Titel

MiR-32-5p/AIDA Mediates OxLDL-Induced Endothelial Injury and Inflammation

Ist Teil von

• International Heart Journal, 2022/09/30, Vol.63(5), pp.928-938

Ort / Verlag

Tokyo: International Heart Journal Association

Erscheinungsjahr

2022

Quelle

EZB Free E-Journals

Beschreibungen/Notizen

• The role of endothelial injury and inflammation in atherosclerosis has been well established. miRNAs have been found to be key regulators in the development of atherosclerosis. Here we investigated whether miR-32-5p and its predicted target gene axin interactor, dorsalization associated (AIDA) are involved in endothelial injury and inflammation. Human umbilical vein endothelial cells (HUVECs) were treated with oxidized low-density lipoprotein (oxLDL) to induce endothelial injury and inflammation. AIDA was predicted to be a target gene of miR-32-5p using TargetScan software. Cell viability, migration, and angiogenesis were evaluated using Cell Counting Kit-8, wound-healing, and tube formation assays, respectively. The expression of inflammatory factors was detected using quantitative PCR, enzyme-linked immunosorbent assay, and western blot. We found that miR-32-5p expression was significantly decreased, whereas AIDA expression was significantly increased in oxLDL-treated HUVECs and the increased AIDA expression was reversed by the up-regulation of miR-32-5p. Moreover, both miR-32-5p mimic and knockdown of AIDA enhanced cell viability, promoted cell migration and angiogenesis and suppressed the expression of inflammatory factors including IL-1β, IL-6, TNF-α, ICAM-1, and VCAM-1 in oxLDL-induced HUVECs. Furthermore, miR-32-5p was verified to directly target AIDA using dual-luciferase reporter assay. Overall, these findings suggest that miR-32-5p/AIDA signal plays an important role in oxLDL-induced endothelial injury and inflammation. This study provides new insights into novel molecular mechanisms of endothelial dysfunction and atherosclerosis.