Dihydroartemisinin up‐regulates VE‐cadherin expression in human renal glomerular endothelial cells

The antimalarial agent dihydroartemisinin (DHA) has been shown to be anti‐inflammatory. In this study, we found that DHA increased the expression of the junctional protein vascular endothelial (VE)‐cadherin in human renal glomerular endothelial cells. In addition, DHA inhibited TGF‐β RI‐Smad2/3 sign...

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Autores principales: Li, Liqun, Chen, Xiaocui, Dong, Fengyun, Liu, Qiang, Zhang, Caiqing, Xu, Dongmei, Allen, Thaddeus D., Liu, Ju
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2017
Materias:
Short Communications
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5824371/
https://www.ncbi.nlm.nih.gov/pubmed/29193726
http://dx.doi.org/10.1111/jcmm.13448
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author Li, Liqun
Chen, Xiaocui
Dong, Fengyun
Liu, Qiang
Zhang, Caiqing
Xu, Dongmei
Allen, Thaddeus D.
Liu, Ju
author_facet Li, Liqun
Chen, Xiaocui
Dong, Fengyun
Liu, Qiang
Zhang, Caiqing
Xu, Dongmei
Allen, Thaddeus D.
Liu, Ju
author_sort Li, Liqun
collection PubMed
description The antimalarial agent dihydroartemisinin (DHA) has been shown to be anti‐inflammatory. In this study, we found that DHA increased the expression of the junctional protein vascular endothelial (VE)‐cadherin in human renal glomerular endothelial cells. In addition, DHA inhibited TGF‐β RI‐Smad2/3 signalling and its downstream effectors SNAIL and SLUG, which repress VE‐cadherin gene transcription. Correspondingly, DHA decreased the binding of SNAIL and SLUG to the VE‐cadherin promoter. Together, our results suggest an effect of DHA in regulating glomerular permeability by elevation of VE‐cadherin expression.
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spelling pubmed-58243712018-03-01 Dihydroartemisinin up‐regulates VE‐cadherin expression in human renal glomerular endothelial cells Li, Liqun Chen, Xiaocui Dong, Fengyun Liu, Qiang Zhang, Caiqing Xu, Dongmei Allen, Thaddeus D. Liu, Ju J Cell Mol Med Short Communications The antimalarial agent dihydroartemisinin (DHA) has been shown to be anti‐inflammatory. In this study, we found that DHA increased the expression of the junctional protein vascular endothelial (VE)‐cadherin in human renal glomerular endothelial cells. In addition, DHA inhibited TGF‐β RI‐Smad2/3 signalling and its downstream effectors SNAIL and SLUG, which repress VE‐cadherin gene transcription. Correspondingly, DHA decreased the binding of SNAIL and SLUG to the VE‐cadherin promoter. Together, our results suggest an effect of DHA in regulating glomerular permeability by elevation of VE‐cadherin expression. John Wiley and Sons Inc. 2017-11-29 2018-03 /pmc/articles/PMC5824371/ /pubmed/29193726 http://dx.doi.org/10.1111/jcmm.13448 Text en © 2017 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Short Communications
Li, Liqun
Chen, Xiaocui
Dong, Fengyun
Liu, Qiang
Zhang, Caiqing
Xu, Dongmei
Allen, Thaddeus D.
Liu, Ju
Dihydroartemisinin up‐regulates VE‐cadherin expression in human renal glomerular endothelial cells
title Dihydroartemisinin up‐regulates VE‐cadherin expression in human renal glomerular endothelial cells
title_full Dihydroartemisinin up‐regulates VE‐cadherin expression in human renal glomerular endothelial cells
title_fullStr Dihydroartemisinin up‐regulates VE‐cadherin expression in human renal glomerular endothelial cells
title_full_unstemmed Dihydroartemisinin up‐regulates VE‐cadherin expression in human renal glomerular endothelial cells
title_short Dihydroartemisinin up‐regulates VE‐cadherin expression in human renal glomerular endothelial cells
title_sort dihydroartemisinin up‐regulates ve‐cadherin expression in human renal glomerular endothelial cells
topic Short Communications
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5824371/
https://www.ncbi.nlm.nih.gov/pubmed/29193726
http://dx.doi.org/10.1111/jcmm.13448
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