Tobacco smoke condensate-induced senescence in endothelial cells was ameliorated by colchicine treatment via suppression of NF-κB and MAPKs P38 and ERK pathways activation
Abstract Smoking is the major cause of cardiovascular diseases and cancer. It induces oxidative stress, leading to DNA damage and cellular senescence. Senescent cells increase the expression and release of pro-inflammatory molecules and matrix metalloproteinase, which are known to play a vital role...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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BMC
2024-04-01
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| Series: | Cell Communication and Signaling |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s12964-024-01594-x |
| _version_ | 1827291447099916288 |
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| author | Dilaware Khan Huakang Zhou Jinliang You Vera Annika Kaiser Rajiv K Khajuria Sajjad Muhammad |
| author_facet | Dilaware Khan Huakang Zhou Jinliang You Vera Annika Kaiser Rajiv K Khajuria Sajjad Muhammad |
| author_sort | Dilaware Khan |
| collection | DOAJ |
| description | Abstract Smoking is the major cause of cardiovascular diseases and cancer. It induces oxidative stress, leading to DNA damage and cellular senescence. Senescent cells increase the expression and release of pro-inflammatory molecules and matrix metalloproteinase, which are known to play a vital role in the initiation and progression of cardiovascular diseases and metastasis in cancer. The current study investigated the smoking induced cellular senescence and employed colchicine that blocked senescence in endothelial cells exposed to tobacco smoke condensate. Colchicine prevented oxidative stress and DNA damage in tobacco smoke-condensate-treated endothelial cells. Colchicin reduced β-gal activity, improved Lamin B1, and attenuated cell growth arrest markers P21 and P53. Colchicine also ameliorated the expression of SASP factors and inhibited the activation of NF-kB and MAPKs P38 and ERK. In summary, colchicine inhibited tobacco smoke condensate-induced senescence in endothelial cells by blocking the activation of NF-kB and MAPKs P38 and ERK. Graphical Abstract |
| first_indexed | 2024-04-24T12:37:11Z |
| format | Article |
| id | doaj.art-50c59c189e184f72b8a88e40cc22deae |
| institution | Directory Open Access Journal |
| issn | 1478-811X |
| language | English |
| last_indexed | 2024-04-24T12:37:11Z |
| publishDate | 2024-04-01 |
| publisher | BMC |
| record_format | Article |
| series | Cell Communication and Signaling |
| spelling | doaj.art-50c59c189e184f72b8a88e40cc22deae2024-04-07T11:25:23ZengBMCCell Communication and Signaling1478-811X2024-04-0122111310.1186/s12964-024-01594-xTobacco smoke condensate-induced senescence in endothelial cells was ameliorated by colchicine treatment via suppression of NF-κB and MAPKs P38 and ERK pathways activationDilaware Khan0Huakang Zhou1Jinliang You2Vera Annika Kaiser3Rajiv K Khajuria4Sajjad Muhammad5Department of Neurosurgery, Medical Faculty, University Hospital Düsseldorf, Heinrich-Heine- Universität DüsseldorfDepartment of Neurosurgery, Medical Faculty, University Hospital Düsseldorf, Heinrich-Heine- Universität DüsseldorfDepartment of Neurosurgery, Medical Faculty, University Hospital Düsseldorf, Heinrich-Heine- Universität DüsseldorfDepartment of Neurosurgery, Medical Faculty, University Hospital Düsseldorf, Heinrich-Heine- Universität DüsseldorfDepartment of Neurosurgery, Medical Faculty, University Hospital Düsseldorf, Heinrich-Heine- Universität DüsseldorfDepartment of Neurosurgery, Medical Faculty, University Hospital Düsseldorf, Heinrich-Heine- Universität DüsseldorfAbstract Smoking is the major cause of cardiovascular diseases and cancer. It induces oxidative stress, leading to DNA damage and cellular senescence. Senescent cells increase the expression and release of pro-inflammatory molecules and matrix metalloproteinase, which are known to play a vital role in the initiation and progression of cardiovascular diseases and metastasis in cancer. The current study investigated the smoking induced cellular senescence and employed colchicine that blocked senescence in endothelial cells exposed to tobacco smoke condensate. Colchicine prevented oxidative stress and DNA damage in tobacco smoke-condensate-treated endothelial cells. Colchicin reduced β-gal activity, improved Lamin B1, and attenuated cell growth arrest markers P21 and P53. Colchicine also ameliorated the expression of SASP factors and inhibited the activation of NF-kB and MAPKs P38 and ERK. In summary, colchicine inhibited tobacco smoke condensate-induced senescence in endothelial cells by blocking the activation of NF-kB and MAPKs P38 and ERK. Graphical Abstracthttps://doi.org/10.1186/s12964-024-01594-xTobacco smokeHUVECsNF-kBMAPKsSenescenceSASP factors |
| spellingShingle | Dilaware Khan Huakang Zhou Jinliang You Vera Annika Kaiser Rajiv K Khajuria Sajjad Muhammad Tobacco smoke condensate-induced senescence in endothelial cells was ameliorated by colchicine treatment via suppression of NF-κB and MAPKs P38 and ERK pathways activation Cell Communication and Signaling Tobacco smoke HUVECs NF-kB MAPKs Senescence SASP factors |
| title | Tobacco smoke condensate-induced senescence in endothelial cells was ameliorated by colchicine treatment via suppression of NF-κB and MAPKs P38 and ERK pathways activation |
| title_full | Tobacco smoke condensate-induced senescence in endothelial cells was ameliorated by colchicine treatment via suppression of NF-κB and MAPKs P38 and ERK pathways activation |
| title_fullStr | Tobacco smoke condensate-induced senescence in endothelial cells was ameliorated by colchicine treatment via suppression of NF-κB and MAPKs P38 and ERK pathways activation |
| title_full_unstemmed | Tobacco smoke condensate-induced senescence in endothelial cells was ameliorated by colchicine treatment via suppression of NF-κB and MAPKs P38 and ERK pathways activation |
| title_short | Tobacco smoke condensate-induced senescence in endothelial cells was ameliorated by colchicine treatment via suppression of NF-κB and MAPKs P38 and ERK pathways activation |
| title_sort | tobacco smoke condensate induced senescence in endothelial cells was ameliorated by colchicine treatment via suppression of nf κb and mapks p38 and erk pathways activation |
| topic | Tobacco smoke HUVECs NF-kB MAPKs Senescence SASP factors |
| url | https://doi.org/10.1186/s12964-024-01594-x |
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