Atorvastatin protects endothelial colony‑forming cells against H2O2‑induced oxidative damage by regulating the expression of annexin A2
| Autor: | Ji‑Hua Li, Da‑Wei Li, Ying‑Di Wang, Guang‑Ren Li |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Cancer Research
Endothelium Atorvastatin Apoptosis Pharmacology Biology medicine.disease_cause Biochemistry endothelial colony-forming cells Genetics medicine Animals Humans MTT assay Endothelial dysfunction Molecular Biology chemistry.chemical_classification Tube formation Reactive oxygen species Endothelial Cells Hydrogen Peroxide Articles atorvastatin medicine.disease annexin A2 Rats Oxidative Stress medicine.anatomical_structure Oncology chemistry Gene Expression Regulation Immunology Molecular Medicine Annexin A2 Oxidative stress medicine.drug |
| Zdroj: | Molecular Medicine Reports |
| ISSN: | 1791-3004 |
| Popis: | Endothelial dysfunction and injury are central events in the pathogenesis of ischemic vascular disorders. Endothelial progenitor cells (EPCs) are mobilized from the bone marrow into the peripheral circulation, where they locate to sites of injured endothelium and are involved in endothelial repair and vascular regeneration. During these processes, EPCs are exposed to oxidative stress, a crucial pathological condition, which occurs during vascular injury and limits the efficacy of EPCs in the repair of injured endothelium. Statins are effective inhibitors of 3‑hydroxy‑3‑methylglutaryl coenzyme A reductase, and are commonly used to manage and prevent ischemic vascular disease by reducing plasma cholesterol levels. In addition to lowering cholesterol, statins have also been reported to exert pleiotropic actions, including anti‑inflammatory and anti‑oxidative activities. The present study aimed to investigate the ability of atorvastatin to protect endothelial colony‑forming cells (ECFCs), a homogeneous subtype of EPCs, from hydrogen peroxide (H2O2)‑induced oxidative damage, and to determine the mechanism underlying this protective action. MTT assay, acridine orange/ethidium bromide staining, reactive oxygen species assay, western blot analysis and tube formation assay were employed. The results demonstrated that H2O2 induced cell death and decreased the tube‑forming ability of the ECFCs, in a concentration‑dependent manner; however, these effects were partially attenuated following administration of atorvastatin. The reversion of the quantitative and qualitative impairment of the H2O2‑treated ECFCs appeared to be mediated by the regulation of annexin A2, as the expression levels of annexin A2 were decreased following treatment with H2O2 and increased following treatment with atorvastatin. These results indicated that annexin A2 may be involved in the H2O2‑induced damage of ECFCs, and in the protective activities of atorvastatin in response to oxidative stress. |
| Databáze: | OpenAIRE |
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