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MARCKS is involved in methylmercury-induced decrease in cell viability and nitric oxide production in EA.hy926 cells
Cuong VAN Dao1, Md Zahorul Islam, Kasumi Sudo
1Department of Veterinary Pharmacology, Joint Faculty of Veterinary Medicine, Kagoshima University, 1-21-24 Korimoto, Kagoshima 890-0065, Japan.
The Journal of Veterinary Medical Science
|June 29, 2016
Summary
Methylmercury (MeHg) exposure harms endothelial cells, impacting functions like migration and nitric oxide (NO) production. The protein myristoylated alanine-rich C kinase substrate (MARCKS) plays a key role in MeHg toxicity.
Area of Science:
- Environmental toxicology
- Cardiovascular research
- Cell biology
Background:
- Methylmercury (MeHg) is a global environmental contaminant linked to cardiovascular disease.
- Mechanisms of MeHg cardiovascular toxicity remain unclear.
- Previous studies showed MeHg increases blood pressure and impairs vasodilation.
Purpose of the Study:
- Investigate MeHg's toxic effects on human endothelial cells (EA.hy926).
- Elucidate the role of myristoylated alanine-rich C kinase substrate (MARCKS) in MeHg toxicity.
Main Methods:
- Exposed EA.hy926 cells to varying MeHg concentrations.
- Assessed cell viability, migration, tube formation, and nitric oxide (NO) production.
- Manipulated MARCKS expression (knockdown and overexpression).
Main Results:
- MeHg decreased cell viability, migration, tube formation, and NO production in a dose-dependent manner.
- MeHg altered MARCKS expression and phosphorylation.
- MARCKS manipulation affected endothelial cell functions and MeHg's toxic impact.
Conclusions:
- MeHg induces toxicity in human endothelial cells.
- MARCKS is involved in endothelial cell functions and MeHg toxicity.
- MARCKS plays a significant role in the adverse effects of MeHg on the cardiovascular system.
