Autophagy activation is required for homocysteine-induced apoptosis in bovine aorta endothelial cells
An elevated level of homocysteine (Hcy) in plasma is an independent risk factor for cardiovascular disease and central nervous system disease. Endothelial dysfunction as a result of apoptosis in endothelial cells is involved in the development and progression of these diseases. In this study, we aim...
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| Published in: | Heliyon 2020-01, Vol.6 (1), p.e03315-e03315, Article e03315 |
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| Main Authors: | , , , |
| Format: | Article |
| Language: | eng |
| Subjects: | |
| Online Access: | Get full text |
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| Summary: | An elevated level of homocysteine (Hcy) in plasma is an independent risk factor for cardiovascular disease and central nervous system disease. Endothelial dysfunction as a result of apoptosis in endothelial cells is involved in the development and progression of these diseases. In this study, we aimed to investigate the effect of autophagy activation by amino acid starvation on Hcy-induced cytotoxicity in bovine aorta endothelial cells (BAECs). Hcy-induced lactate dehydrogenase (LDH) release was promoted by amino acid starvation. In addition, Hcy increased cleaved caspase-3 level, an indicator of apoptosis, by amino acid starvation. We revealed that oxidative stress is not involved in the Hcy-induced cytotoxicity promoted by amino acid starvation. Salazosulfapyridine (SASP), an SLC7A11 inhibitor, protected against the Hcy-induced LDH release promoted by amino acid starvation. SASP decreased the Hcy-induced cleaved caspase-3 level by amino acid starvation. We demonstrate for the first time that autophagy activation by amino acid starvation promotes Hcy-induced apoptosis in BAECs. Moreover, SLC7A11 inhibitor SASP, which is an amino acid transporter, protects against Hcy-induced apoptosis due to autophagy.
Biological sciences; Cell biology; Cell death; Cytotoxicity; Biochemistry; Oxidative stress; Antioxidant; Toxicology; Homocysteine; Bovine aorta endothelial cell; Autophagy; Apoptosis; SLC7A11 |
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| ISSN: | 2405-8440 2405-8440 |