Oscillatory Shear Stress Induces Oxidative Stress via TLR4 Activation in Endothelial Cells
Background. Oscillatory shear stress (OSS) disrupts endothelial homeostasis and promotes oxidative stress, which can lead to atherosclerosis. In atherosclerotic lesions, Toll-like receptor 4 (TLR4) is highly expressed. However, the molecular mechanism by which TLR4 modulates oxidative changes and th...
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| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2019-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2019/7162976 |
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| _version_ | 1832559414113992704 |
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| author | Zhimei Wang Feng Wang Xiangquan Kong Xiaofei Gao Yue Gu Junjie Zhang |
| author_facet | Zhimei Wang Feng Wang Xiangquan Kong Xiaofei Gao Yue Gu Junjie Zhang |
| author_sort | Zhimei Wang |
| collection | DOAJ |
| description | Background. Oscillatory shear stress (OSS) disrupts endothelial homeostasis and promotes oxidative stress, which can lead to atherosclerosis. In atherosclerotic lesions, Toll-like receptor 4 (TLR4) is highly expressed. However, the molecular mechanism by which TLR4 modulates oxidative changes and the cell signaling transudation upon OSS is yet to be determined. Methods and Results. Carotid artery constriction (CAC) surgery and a parallel-plate flow chamber were used to modulate shear stress. The results showed that OSS significantly increased the oxidative burden, and this was partly due to TLR4 activation. OSS activated NOX2 and had no significant influence to NOX1 or NOX4 in endothelial cells (ECs). OSS phosphorylated caveolin-1, promoted its binding with endothelial nitric oxide synthase (eNOS), and resulted in deactivation of eNOS. TLR4 inhibition restored levels of nitric oxide (NO) and superoxide dismutase (SOD) in OSS-exposed cells. Conclusion. TLR4 modulates OSS-induced oxidative stress by activating NOX2 and suppressing eNOS. |
| format | Article |
| id | doaj-art-4f9ad9956e5d4e9292dcb90f8069e85b |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2019-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-4f9ad9956e5d4e9292dcb90f8069e85b2025-02-03T01:30:06ZengWileyMediators of Inflammation0962-93511466-18612019-01-01201910.1155/2019/71629767162976Oscillatory Shear Stress Induces Oxidative Stress via TLR4 Activation in Endothelial CellsZhimei Wang0Feng Wang1Xiangquan Kong2Xiaofei Gao3Yue Gu4Junjie Zhang5Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, ChinaDepartment of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, ChinaDepartment of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, ChinaDepartment of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, ChinaDepartment of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, ChinaDepartment of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, ChinaBackground. Oscillatory shear stress (OSS) disrupts endothelial homeostasis and promotes oxidative stress, which can lead to atherosclerosis. In atherosclerotic lesions, Toll-like receptor 4 (TLR4) is highly expressed. However, the molecular mechanism by which TLR4 modulates oxidative changes and the cell signaling transudation upon OSS is yet to be determined. Methods and Results. Carotid artery constriction (CAC) surgery and a parallel-plate flow chamber were used to modulate shear stress. The results showed that OSS significantly increased the oxidative burden, and this was partly due to TLR4 activation. OSS activated NOX2 and had no significant influence to NOX1 or NOX4 in endothelial cells (ECs). OSS phosphorylated caveolin-1, promoted its binding with endothelial nitric oxide synthase (eNOS), and resulted in deactivation of eNOS. TLR4 inhibition restored levels of nitric oxide (NO) and superoxide dismutase (SOD) in OSS-exposed cells. Conclusion. TLR4 modulates OSS-induced oxidative stress by activating NOX2 and suppressing eNOS.http://dx.doi.org/10.1155/2019/7162976 |
| spellingShingle | Zhimei Wang Feng Wang Xiangquan Kong Xiaofei Gao Yue Gu Junjie Zhang Oscillatory Shear Stress Induces Oxidative Stress via TLR4 Activation in Endothelial Cells Mediators of Inflammation |
| title | Oscillatory Shear Stress Induces Oxidative Stress via TLR4 Activation in Endothelial Cells |
| title_full | Oscillatory Shear Stress Induces Oxidative Stress via TLR4 Activation in Endothelial Cells |
| title_fullStr | Oscillatory Shear Stress Induces Oxidative Stress via TLR4 Activation in Endothelial Cells |
| title_full_unstemmed | Oscillatory Shear Stress Induces Oxidative Stress via TLR4 Activation in Endothelial Cells |
| title_short | Oscillatory Shear Stress Induces Oxidative Stress via TLR4 Activation in Endothelial Cells |
| title_sort | oscillatory shear stress induces oxidative stress via tlr4 activation in endothelial cells |
| url | http://dx.doi.org/10.1155/2019/7162976 |
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