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Tetrahydroxy stilbene glycoside attenuates endothelial cell premature senescence induced by H(2)O(2) through the microRNA-34a/SIRT1 pathway

Numerous studies have demonstrated that endothelial cell senescence plays a decisive role in the development and progression of cardiovascular diseases (CVD). Our previous results confirmed that Tetrahydroxy stilbene glycoside (TSG) can alleviate the human umbilical vein endothelial cells (HUVECs) s...

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Autores principales: Zhang, Lixuan, Guo, Yan, Shi, Shennan, Zhuge, Yani, Chen, Nipi, Ding, Zhishan, Jin, Bo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8807705/
https://www.ncbi.nlm.nih.gov/pubmed/35105933
http://dx.doi.org/10.1038/s41598-022-05804-9
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author Zhang, Lixuan
Guo, Yan
Shi, Shennan
Zhuge, Yani
Chen, Nipi
Ding, Zhishan
Jin, Bo
author_facet Zhang, Lixuan
Guo, Yan
Shi, Shennan
Zhuge, Yani
Chen, Nipi
Ding, Zhishan
Jin, Bo
author_sort Zhang, Lixuan
collection PubMed
description Numerous studies have demonstrated that endothelial cell senescence plays a decisive role in the development and progression of cardiovascular diseases (CVD). Our previous results confirmed that Tetrahydroxy stilbene glycoside (TSG) can alleviate the human umbilical vein endothelial cells (HUVECs) senescence induced by H(2)O(2) through SIRT1. It has been reported that miR-34a is a translational suppressor of SIRT1. In this study, we aimed to explore whether TSG regulates SIRT1 through miR-34a to ameliorate HUVECs senescence. H(2)O(2) was used to induce premature senescence in HUVECs, and miR-34a mimic or inhibitor were transfected to over-express or suppress the expression level of miR-34a. Results revealed that TSG apparently decreased the miR-34a expression level in H(2)O(2)-induced premature senescence of HUVECs. When SIRT1 expression was inhibited by EX527, the attenuation of TSG on the expression level of miR-34a were abolished. When miR-34a expression was knockdown, the effect of TSG on HUVECs senescence could be enhanced. While miR-34a mimic could reverse the effect of TSG on HUVECs senescence. In conclusion, we demonstrated that TSG could attenuated endothelial cell senescence by targeting miR-34a/SIRT1 pathway.
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spelling pubmed-88077052022-02-03 Tetrahydroxy stilbene glycoside attenuates endothelial cell premature senescence induced by H(2)O(2) through the microRNA-34a/SIRT1 pathway Zhang, Lixuan Guo, Yan Shi, Shennan Zhuge, Yani Chen, Nipi Ding, Zhishan Jin, Bo Sci Rep Article Numerous studies have demonstrated that endothelial cell senescence plays a decisive role in the development and progression of cardiovascular diseases (CVD). Our previous results confirmed that Tetrahydroxy stilbene glycoside (TSG) can alleviate the human umbilical vein endothelial cells (HUVECs) senescence induced by H(2)O(2) through SIRT1. It has been reported that miR-34a is a translational suppressor of SIRT1. In this study, we aimed to explore whether TSG regulates SIRT1 through miR-34a to ameliorate HUVECs senescence. H(2)O(2) was used to induce premature senescence in HUVECs, and miR-34a mimic or inhibitor were transfected to over-express or suppress the expression level of miR-34a. Results revealed that TSG apparently decreased the miR-34a expression level in H(2)O(2)-induced premature senescence of HUVECs. When SIRT1 expression was inhibited by EX527, the attenuation of TSG on the expression level of miR-34a were abolished. When miR-34a expression was knockdown, the effect of TSG on HUVECs senescence could be enhanced. While miR-34a mimic could reverse the effect of TSG on HUVECs senescence. In conclusion, we demonstrated that TSG could attenuated endothelial cell senescence by targeting miR-34a/SIRT1 pathway. Nature Publishing Group UK 2022-02-01 /pmc/articles/PMC8807705/ /pubmed/35105933 http://dx.doi.org/10.1038/s41598-022-05804-9 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Zhang, Lixuan
Guo, Yan
Shi, Shennan
Zhuge, Yani
Chen, Nipi
Ding, Zhishan
Jin, Bo
Tetrahydroxy stilbene glycoside attenuates endothelial cell premature senescence induced by H(2)O(2) through the microRNA-34a/SIRT1 pathway
title Tetrahydroxy stilbene glycoside attenuates endothelial cell premature senescence induced by H(2)O(2) through the microRNA-34a/SIRT1 pathway
title_full Tetrahydroxy stilbene glycoside attenuates endothelial cell premature senescence induced by H(2)O(2) through the microRNA-34a/SIRT1 pathway
title_fullStr Tetrahydroxy stilbene glycoside attenuates endothelial cell premature senescence induced by H(2)O(2) through the microRNA-34a/SIRT1 pathway
title_full_unstemmed Tetrahydroxy stilbene glycoside attenuates endothelial cell premature senescence induced by H(2)O(2) through the microRNA-34a/SIRT1 pathway
title_short Tetrahydroxy stilbene glycoside attenuates endothelial cell premature senescence induced by H(2)O(2) through the microRNA-34a/SIRT1 pathway
title_sort tetrahydroxy stilbene glycoside attenuates endothelial cell premature senescence induced by h(2)o(2) through the microrna-34a/sirt1 pathway
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8807705/
https://www.ncbi.nlm.nih.gov/pubmed/35105933
http://dx.doi.org/10.1038/s41598-022-05804-9
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