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Angiotensin II inhibits ZO-1 expression in endothelial cells by down-regulating VE-cadherin |
SHEN Hongfeng, CHA Wei, JIN Zhijiang, XIA Haijiang, LIU Longbin. |
Department of Cardiology, the Affiliated Hospital of Shaoxing University, Shaoxing Municipal Hospital, Shaoxing 312000, China |
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Cite this article: |
SHEN Hongfeng,CHA Wei,JIN Zhijiang, et al. Angiotensin II inhibits ZO-1 expression in endothelial cells by down-regulating VE-cadherin[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2023, 53(9): 729-733.
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Abstract Objective: To explore the mechanism by which angiotensin (Ang II) disrupts microvascular permeability. Methods: The primary culture and identification of rat endothelial cells were conducted, and cells in passage 4-7 used for the experiment were divided as the control, Ang II and Ang II+valsartan groups; real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot were used to test the expression of zonula occludens-1 (ZO-1) and vascular endothelial (VE)-cadherin in the cells; the distribution of ZO-1 protein was detected by immunofluorescence assay. After transfection of VE-cadherin into endothelial cells, the cells were
divided as the control, Ang II and Ang II+VE-cadherin groups. The expression and distribution of ZO-1 protein were also detected. Results: Compared with the control group, the expression of ZO-1 and VE-cadherin in Ang II group was significantly decreased in mRNA level and protein level (both P<0.01). Additionally, the peripheral
positioning of ZO-1 protein in cell membrane was remarkably depressed. However, over-expression of VEcadherin by transfecting over-expression plasmid could significantly reverse the expression and distribution of ZO-1 in Ang II-treated endothelial cells. Conclusion: Ang II inhibited the expression of ZO-1 protein in vascular
endothelial cells by down-regulating VE-cadherin, thus destroying the tight junction between endothelial cells,which may be the possible mechanism by which Ang II disrupts microvascular permeability.
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Received: 22 February 2023
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