YTHDF1 silencing significantly attenuated ox-LDL-induced endothelial injury in human coronary artery endothelial cells by decreasing BACH1 mRNA translation in an m6A-dependent manner (p<0.05).
Does YTHDF1 silencing mitigate ox-LDL-induced endothelial dysfunction in human coronary artery endothelial cells?
YTHDF1 depletion mitigates ox-LDL-induced endothelial dysfunction by decreasing BACH1 mRNA translation, suggesting a potential novel therapeutic target for coronary heart disease.
p-value: p=<0.05
Background: Endothelial dysfunction is a pivotal contributor to coronary heart disease (CHD). The study aimed to elucidate the involvement of YT521-B homology domain 1 (YTHDF1) in mediating endothelial dysfunction triggered by oxidized low-density lipoprotein (ox-LDL) in human coronary artery endothelial cells (HCAECs). Methods: Cell viability was evaluated using the Cell Counting Kit-8 (CCK-8) assay, while apoptotic status was determined by flow cytometric analysis. Cell migratory capacity was examined through a Transwell assay. The concentrations of pro-inflammatory cytokines (Tumor necrosis factor (TNF)-α, Interleukin (IL)-1β, and IL-18) together with the adhesion molecule VCAM-1 were measured using Enzyme-linked immunosorbent assay (ELISA). Intracellular Reactive oxygen species (ROS) production was assessed via DCFH-DA fluorescent staining. The N6-methyladenosine (m6A) modification level of BTB and CNC homology 1 (BACH1) was analyzed using Methylated RNA binding protein immunoprecipitation (MeRIP), and molecular interactions were further explored using RNA binding protein immunoprecipitation (RIP) assay. Results: YTHDF1 expression was significantly increased in peripheral blood mononuclear cells (PBMCs) from CHD patients compared with healthy controls and in ox-LDL-treated HCAECs compared with untreated cells (p p 6A-dependent manner (p p 6A-dependent manner.
Fang et al. (Thu,) conducted a other in Coronary heart disease and endothelial dysfunction. YTHDF1 silencing vs. Untreated cells / BACH1 overexpression was evaluated on Endothelial injury (cell viability, apoptosis, migration, inflammatory cytokines, ROS production) (p=<0.05). YTHDF1 silencing significantly attenuated ox-LDL-induced endothelial injury in human coronary artery endothelial cells by decreasing BACH1 mRNA translation in an m6A-dependent manner (p<0.05).