Shear stress leads to the dysfunction of endothelial cells through the Cav-1-mediated KLF2/eNOS/ERK signaling pathway under physiological conditions
To investigate the mechanism of shear stress on endothelial cell dysfunction for providing a theoretical basis for the reduction of arteriovenous fistula dysfunction. The in vitro parallel plate flow chamber was used to form different forces and shear stress to mimic the hemodynamic changes in human...
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| Format: | Article |
| Language: | English |
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De Gruyter
2023-04-01
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| Series: | Open Life Sciences |
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| Online Access: | https://doi.org/10.1515/biol-2022-0587 |
| _version_ | 1797832526164656128 |
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| author | Wang Lihua Wang Bingyue Jia Lan Yu Haibo Wang Zhe Wei Fang Jiang Aili |
| author_facet | Wang Lihua Wang Bingyue Jia Lan Yu Haibo Wang Zhe Wei Fang Jiang Aili |
| author_sort | Wang Lihua |
| collection | DOAJ |
| description | To investigate the mechanism of shear stress on endothelial cell dysfunction for providing a theoretical basis for the reduction of arteriovenous fistula dysfunction. The in vitro parallel plate flow chamber was used to form different forces and shear stress to mimic the hemodynamic changes in human umbilical vein endothelial cells, and the expression and distribution of krüppel-like factor 2 (KLF2), caveolin-1 (Cav-1), p-extracellular regulated protein kinase (p-ERK), and endothelial nitric oxide synthase (eNOS) were detected by immunofluorescence and real-time quantitative polymerase chain reaction. With the prolongation of the shear stress action time, the expression of KLF2 and eNOS increased gradually, while the expression of Cav-1 and p-ERK decreased gradually. In addition, after cells were exposed to oscillatory shear stress (OSS) and low shear stress, the expression of KLF2, Cav-1, and eNOS decreased and the expression of p-ERK increased. The expression of KLF2 increased gradually with the prolongation of action time, but it was still obviously lower than that of high shear stress. Following the block of Cav-1 expression by methyl β-cyclodextrin, eNOS expression decreased, and KLF2 and p-ERK expression increased. OSS may lead to endothelial cell dysfunction by Cav-1-mediated KLF2/eNOS/ERK signaling pathway. |
| first_indexed | 2024-04-09T14:09:19Z |
| format | Article |
| id | doaj.art-f1d2d24465b94285bd043763903d3281 |
| institution | Directory Open Access Journal |
| issn | 2391-5412 |
| language | English |
| last_indexed | 2024-04-09T14:09:19Z |
| publishDate | 2023-04-01 |
| publisher | De Gruyter |
| record_format | Article |
| series | Open Life Sciences |
| spelling | doaj.art-f1d2d24465b94285bd043763903d32812023-05-06T15:42:46ZengDe GruyterOpen Life Sciences2391-54122023-04-011814263110.1515/biol-2022-0587Shear stress leads to the dysfunction of endothelial cells through the Cav-1-mediated KLF2/eNOS/ERK signaling pathway under physiological conditionsWang Lihua0Wang Bingyue1Jia Lan2Yu Haibo3Wang Zhe4Wei Fang5Jiang Aili6Department of Kidney Disease and Blood Purification Centre, 2nd Hospital of Tianjin Medical University, 23rd, Pingjiang Road, Hexi District, Tianjin300211, ChinaBlood Purification Center of Tianjin Third Central Hospital, Tianjin300170, ChinaDepartment of Kidney Disease and Blood Purification Centre, 2nd Hospital of Tianjin Medical University, 23rd, Pingjiang Road, Hexi District, Tianjin300211, ChinaDepartment of Kidney Disease and Blood Purification Centre, 2nd Hospital of Tianjin Medical University, 23rd, Pingjiang Road, Hexi District, Tianjin300211, ChinaDepartment of Kidney Disease and Blood Purification Centre, 2nd Hospital of Tianjin Medical University, 23rd, Pingjiang Road, Hexi District, Tianjin300211, ChinaDepartment of Kidney Disease and Blood Purification Centre, 2nd Hospital of Tianjin Medical University, 23rd, Pingjiang Road, Hexi District, Tianjin300211, ChinaDepartment of Kidney Disease and Blood Purification Centre, 2nd Hospital of Tianjin Medical University, 23rd, Pingjiang Road, Hexi District, Tianjin300211, ChinaTo investigate the mechanism of shear stress on endothelial cell dysfunction for providing a theoretical basis for the reduction of arteriovenous fistula dysfunction. The in vitro parallel plate flow chamber was used to form different forces and shear stress to mimic the hemodynamic changes in human umbilical vein endothelial cells, and the expression and distribution of krüppel-like factor 2 (KLF2), caveolin-1 (Cav-1), p-extracellular regulated protein kinase (p-ERK), and endothelial nitric oxide synthase (eNOS) were detected by immunofluorescence and real-time quantitative polymerase chain reaction. With the prolongation of the shear stress action time, the expression of KLF2 and eNOS increased gradually, while the expression of Cav-1 and p-ERK decreased gradually. In addition, after cells were exposed to oscillatory shear stress (OSS) and low shear stress, the expression of KLF2, Cav-1, and eNOS decreased and the expression of p-ERK increased. The expression of KLF2 increased gradually with the prolongation of action time, but it was still obviously lower than that of high shear stress. Following the block of Cav-1 expression by methyl β-cyclodextrin, eNOS expression decreased, and KLF2 and p-ERK expression increased. OSS may lead to endothelial cell dysfunction by Cav-1-mediated KLF2/eNOS/ERK signaling pathway.https://doi.org/10.1515/biol-2022-0587shear stressdysfunctionendothelial cellsextracellular regulated protein kinasekrüppel-like factor 2caveolin-1 |
| spellingShingle | Wang Lihua Wang Bingyue Jia Lan Yu Haibo Wang Zhe Wei Fang Jiang Aili Shear stress leads to the dysfunction of endothelial cells through the Cav-1-mediated KLF2/eNOS/ERK signaling pathway under physiological conditions Open Life Sciences shear stress dysfunction endothelial cells extracellular regulated protein kinase krüppel-like factor 2 caveolin-1 |
| title | Shear stress leads to the dysfunction of endothelial cells through the Cav-1-mediated KLF2/eNOS/ERK signaling pathway under physiological conditions |
| title_full | Shear stress leads to the dysfunction of endothelial cells through the Cav-1-mediated KLF2/eNOS/ERK signaling pathway under physiological conditions |
| title_fullStr | Shear stress leads to the dysfunction of endothelial cells through the Cav-1-mediated KLF2/eNOS/ERK signaling pathway under physiological conditions |
| title_full_unstemmed | Shear stress leads to the dysfunction of endothelial cells through the Cav-1-mediated KLF2/eNOS/ERK signaling pathway under physiological conditions |
| title_short | Shear stress leads to the dysfunction of endothelial cells through the Cav-1-mediated KLF2/eNOS/ERK signaling pathway under physiological conditions |
| title_sort | shear stress leads to the dysfunction of endothelial cells through the cav 1 mediated klf2 enos erk signaling pathway under physiological conditions |
| topic | shear stress dysfunction endothelial cells extracellular regulated protein kinase krüppel-like factor 2 caveolin-1 |
| url | https://doi.org/10.1515/biol-2022-0587 |
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