Homocysteine induces ferroptosis in endothelial cells through the systemXc - /GPX4 signaling pathway

• Published in: BMC cardiovascular disorders 2023-06, Vol.23 (1), p.316-316, Article 316
• Main Authors: Shi, Jiahao, Zhang, Shuying, Chen, Di, Li, Shaolin, Wang, Zilin
• Format: Article
• Language: English
• Subjects: Analysis; Antibodies; Apoptosis; Atherosclerosis; Care and treatment; Cell culture; Cell death; Cell proliferation; Cell viability; Cells; Cholecystokinin; Diagnosis; Endothelial Cells; Ferroptosis; Flow cytometry; Health aspects; Homocysteine; Homocysteine - toxicity; Humans; Lipid peroxidation; Lipids; Oxidative stress; Protein expression; Proteins; Reactive Oxygen Species; Signal Transduction; Statistical analysis; Statistical significance; SystemXc−/GPX4 signaling pathway; Vascular endothelial cells; Western blotting
• ISSN: 1471-2261; 1471-2261
• DOI: 10.1186/s12872-023-03342-4

To investigate whether ferroptosis is involved in HCY-induced endothelial injury and the possible mechanism of HCY-induced ferroptosis. EA. hy926 cells were cultured in vitro. Cells were intervened using HCY and Fer-1. The cells were divided into Control groups, HCY (4 mM), HCY (8 mM), HCY + Fer-1 (4 mM HCY + 0.5/2.5/5 µM Fer-1). CCK-8 assay was used to detect cell viability; Flow Cytometry was used to detect cellular Lip-ROS, TBA and Microplate assay was used to detect MDA&GSH, Western blot was used to detect the expression of ferroptosis-related proteins GPX4 and SLC7A11. HCY can inhibited the proliferation of EA. hy926 cells in a time- and concentration-dependent manner; Fer-1 inhibits HCY-induced ferroptosis in EA.hy926 cells in a concentration-dependent manner; Compared with the control group, the cell viability and GSH content in the HCY group was significantly decreased (p