Colchicine Protects against Ethanol-Induced Senescence and Senescence-Associated Secretory Phenotype in Endothelial Cells
Inflammaging is a potential risk factor for cardiovascular diseases. It results in the development of thrombosis and atherosclerosis. The accumulation of senescent cells in vessels causes vascular inflammaging and contributes to plaque formation and rupture. In addition to being an acquired risk fac...
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MDPI AG
2023-04-01
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Series: | Antioxidants |
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Online Access: | https://www.mdpi.com/2076-3921/12/4/960 |
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author | Huakang Zhou Dilaware Khan Norbert Gerdes Carsten Hagenbeck Majeed Rana Jan Frederick Cornelius Sajjad Muhammad |
author_facet | Huakang Zhou Dilaware Khan Norbert Gerdes Carsten Hagenbeck Majeed Rana Jan Frederick Cornelius Sajjad Muhammad |
author_sort | Huakang Zhou |
collection | DOAJ |
description | Inflammaging is a potential risk factor for cardiovascular diseases. It results in the development of thrombosis and atherosclerosis. The accumulation of senescent cells in vessels causes vascular inflammaging and contributes to plaque formation and rupture. In addition to being an acquired risk factor for cardiovascular diseases, ethanol can induce inflammation and senescence, both of which have been implicated in cardiovascular diseases. In the current study, we used colchicine to abate the cellular damaging effects of ethanol on endothelial cells. Colchicine prevented senescence and averted oxidative stress in endothelial cells exposed to ethanol. It lowered the relative protein expression of aging and senescence marker P21 and restored expression of the DNA repair proteins KU70/KU80. Colchicine inhibited the activation of nuclear factor kappa B (NFκ-B) and mitogen activated protein kinases (MAPKs) in ethanol-treated endothelial cells. It reduced ethanol-induced senescence-associated secretory phenotype. In summary, we show that colchicine ameliorated the ethanol-caused molecular events, resulting in attenuated senescence and senescence-associated secretory phenotype in endothelial cells. |
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issn | 2076-3921 |
language | English |
last_indexed | 2024-03-11T05:17:55Z |
publishDate | 2023-04-01 |
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spelling | doaj.art-5b7652c2675545558b7ed0cf151d86e92023-11-17T18:06:52ZengMDPI AGAntioxidants2076-39212023-04-0112496010.3390/antiox12040960Colchicine Protects against Ethanol-Induced Senescence and Senescence-Associated Secretory Phenotype in Endothelial CellsHuakang Zhou0Dilaware Khan1Norbert Gerdes2Carsten Hagenbeck3Majeed Rana4Jan Frederick Cornelius5Sajjad Muhammad6Department of Neurosurgery, Medical Faculty and University Hospital Düsseldorf, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, GermanyDepartment of Neurosurgery, Medical Faculty and University Hospital Düsseldorf, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, GermanyDivision of Cardiology, Pulmonology and Vascular Medicine, University Hospital and Medical Faculty, Heinrich-Heine-University, 40225 Düsseldorf, GermanyClinic for Gynecology and Obstetrics, University Clinic, 40225 Düsseldorf, GermanyDepartment of Oral, Maxillofacial and Facial Plastic Surgery, University Hospital Düsseldorf, Moorenstrasse 5, 40225 Düsseldorf, GermanyDepartment of Neurosurgery, Medical Faculty and University Hospital Düsseldorf, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, GermanyDepartment of Neurosurgery, Medical Faculty and University Hospital Düsseldorf, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, GermanyInflammaging is a potential risk factor for cardiovascular diseases. It results in the development of thrombosis and atherosclerosis. The accumulation of senescent cells in vessels causes vascular inflammaging and contributes to plaque formation and rupture. In addition to being an acquired risk factor for cardiovascular diseases, ethanol can induce inflammation and senescence, both of which have been implicated in cardiovascular diseases. In the current study, we used colchicine to abate the cellular damaging effects of ethanol on endothelial cells. Colchicine prevented senescence and averted oxidative stress in endothelial cells exposed to ethanol. It lowered the relative protein expression of aging and senescence marker P21 and restored expression of the DNA repair proteins KU70/KU80. Colchicine inhibited the activation of nuclear factor kappa B (NFκ-B) and mitogen activated protein kinases (MAPKs) in ethanol-treated endothelial cells. It reduced ethanol-induced senescence-associated secretory phenotype. In summary, we show that colchicine ameliorated the ethanol-caused molecular events, resulting in attenuated senescence and senescence-associated secretory phenotype in endothelial cells.https://www.mdpi.com/2076-3921/12/4/960ethanolHUVECscellular senescenceSASPinflammationcolchicine |
spellingShingle | Huakang Zhou Dilaware Khan Norbert Gerdes Carsten Hagenbeck Majeed Rana Jan Frederick Cornelius Sajjad Muhammad Colchicine Protects against Ethanol-Induced Senescence and Senescence-Associated Secretory Phenotype in Endothelial Cells Antioxidants ethanol HUVECs cellular senescence SASP inflammation colchicine |
title | Colchicine Protects against Ethanol-Induced Senescence and Senescence-Associated Secretory Phenotype in Endothelial Cells |
title_full | Colchicine Protects against Ethanol-Induced Senescence and Senescence-Associated Secretory Phenotype in Endothelial Cells |
title_fullStr | Colchicine Protects against Ethanol-Induced Senescence and Senescence-Associated Secretory Phenotype in Endothelial Cells |
title_full_unstemmed | Colchicine Protects against Ethanol-Induced Senescence and Senescence-Associated Secretory Phenotype in Endothelial Cells |
title_short | Colchicine Protects against Ethanol-Induced Senescence and Senescence-Associated Secretory Phenotype in Endothelial Cells |
title_sort | colchicine protects against ethanol induced senescence and senescence associated secretory phenotype in endothelial cells |
topic | ethanol HUVECs cellular senescence SASP inflammation colchicine |
url | https://www.mdpi.com/2076-3921/12/4/960 |
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