Cargando…
Dihydromyricetin Attenuates TNF-α-Induced Endothelial Dysfunction through miR-21-Mediated DDAH1/ADMA/NO Signal Pathway
Accumulating studies demonstrate that dihydromyricetin (DMY), a compound extracted from Chinese traditional herb, Ampelopsis grossedentata, attenuates atherosclerotic process by improvement of endothelial dysfunction. However, the underlying mechanism remains poorly understood. Thus, the aim of this...
Autores principales: | , , , , , , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2018
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5850903/ https://www.ncbi.nlm.nih.gov/pubmed/29682517 http://dx.doi.org/10.1155/2018/1047810 |
_version_ | 1783306304907902976 |
---|---|
author | Yang, Dafeng Tan, Shenglan Yang, Zhousheng Jiang, Pei Qin, Caie Yuan, Qiong Dang, Ruili Yao, Xiaoxia Qu, Jian Lu, Qiong Xu, Ping Zhang, Bikui Xiang, Daxiong Chen, Lei |
author_facet | Yang, Dafeng Tan, Shenglan Yang, Zhousheng Jiang, Pei Qin, Caie Yuan, Qiong Dang, Ruili Yao, Xiaoxia Qu, Jian Lu, Qiong Xu, Ping Zhang, Bikui Xiang, Daxiong Chen, Lei |
author_sort | Yang, Dafeng |
collection | PubMed |
description | Accumulating studies demonstrate that dihydromyricetin (DMY), a compound extracted from Chinese traditional herb, Ampelopsis grossedentata, attenuates atherosclerotic process by improvement of endothelial dysfunction. However, the underlying mechanism remains poorly understood. Thus, the aim of this study is to investigate the potential mechanism behind the attenuating effects of DMY on tumor necrosis factor alpha- (TNF-α-) induced endothelial dysfunction. In response to TNF-α, microRNA-21 (miR-21) expression was significantly increased in human umbilical vein endothelial cells (HUVECs), in line with impaired endothelial dysfunction as evidenced by decreased tube formation and migration, endothelial nitric oxide synthase (eNOS) (ser1177) phosphorylation, dimethylarginine dimethylaminohydrolases 1 (DDAH1) expression and metabolic activity, and nitric oxide (NO) concentration as well as increased asymmetric dimethylarginine (ADMA) levels. In contrast, DMY or blockade of miR-21 expression ameliorated endothelial dysfunction in HUVECs treated with TNF-α through downregulation of miR-21 expression, whereas these effects were abolished by overexpression of miR-21. In addition, using a nonspecific NOS inhibitor, L-NAME, also abrogated the attenuating effects of DMY on endothelial dysfunction. Taken together, these data demonstrated that miR-21-mediated DDAH1/ADMA/NO signal pathway plays an important role in TNF-α-induced endothelial dysfunction, and DMY attenuated endothelial dysfunction induced by TNF-α in a miR-21-dependent manner. |
format | Online Article Text |
id | pubmed-5850903 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-58509032018-04-22 Dihydromyricetin Attenuates TNF-α-Induced Endothelial Dysfunction through miR-21-Mediated DDAH1/ADMA/NO Signal Pathway Yang, Dafeng Tan, Shenglan Yang, Zhousheng Jiang, Pei Qin, Caie Yuan, Qiong Dang, Ruili Yao, Xiaoxia Qu, Jian Lu, Qiong Xu, Ping Zhang, Bikui Xiang, Daxiong Chen, Lei Biomed Res Int Research Article Accumulating studies demonstrate that dihydromyricetin (DMY), a compound extracted from Chinese traditional herb, Ampelopsis grossedentata, attenuates atherosclerotic process by improvement of endothelial dysfunction. However, the underlying mechanism remains poorly understood. Thus, the aim of this study is to investigate the potential mechanism behind the attenuating effects of DMY on tumor necrosis factor alpha- (TNF-α-) induced endothelial dysfunction. In response to TNF-α, microRNA-21 (miR-21) expression was significantly increased in human umbilical vein endothelial cells (HUVECs), in line with impaired endothelial dysfunction as evidenced by decreased tube formation and migration, endothelial nitric oxide synthase (eNOS) (ser1177) phosphorylation, dimethylarginine dimethylaminohydrolases 1 (DDAH1) expression and metabolic activity, and nitric oxide (NO) concentration as well as increased asymmetric dimethylarginine (ADMA) levels. In contrast, DMY or blockade of miR-21 expression ameliorated endothelial dysfunction in HUVECs treated with TNF-α through downregulation of miR-21 expression, whereas these effects were abolished by overexpression of miR-21. In addition, using a nonspecific NOS inhibitor, L-NAME, also abrogated the attenuating effects of DMY on endothelial dysfunction. Taken together, these data demonstrated that miR-21-mediated DDAH1/ADMA/NO signal pathway plays an important role in TNF-α-induced endothelial dysfunction, and DMY attenuated endothelial dysfunction induced by TNF-α in a miR-21-dependent manner. Hindawi 2018-02-28 /pmc/articles/PMC5850903/ /pubmed/29682517 http://dx.doi.org/10.1155/2018/1047810 Text en Copyright © 2018 Dafeng Yang et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Yang, Dafeng Tan, Shenglan Yang, Zhousheng Jiang, Pei Qin, Caie Yuan, Qiong Dang, Ruili Yao, Xiaoxia Qu, Jian Lu, Qiong Xu, Ping Zhang, Bikui Xiang, Daxiong Chen, Lei Dihydromyricetin Attenuates TNF-α-Induced Endothelial Dysfunction through miR-21-Mediated DDAH1/ADMA/NO Signal Pathway |
title | Dihydromyricetin Attenuates TNF-α-Induced Endothelial Dysfunction through miR-21-Mediated DDAH1/ADMA/NO Signal Pathway |
title_full | Dihydromyricetin Attenuates TNF-α-Induced Endothelial Dysfunction through miR-21-Mediated DDAH1/ADMA/NO Signal Pathway |
title_fullStr | Dihydromyricetin Attenuates TNF-α-Induced Endothelial Dysfunction through miR-21-Mediated DDAH1/ADMA/NO Signal Pathway |
title_full_unstemmed | Dihydromyricetin Attenuates TNF-α-Induced Endothelial Dysfunction through miR-21-Mediated DDAH1/ADMA/NO Signal Pathway |
title_short | Dihydromyricetin Attenuates TNF-α-Induced Endothelial Dysfunction through miR-21-Mediated DDAH1/ADMA/NO Signal Pathway |
title_sort | dihydromyricetin attenuates tnf-α-induced endothelial dysfunction through mir-21-mediated ddah1/adma/no signal pathway |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5850903/ https://www.ncbi.nlm.nih.gov/pubmed/29682517 http://dx.doi.org/10.1155/2018/1047810 |
work_keys_str_mv | AT yangdafeng dihydromyricetinattenuatestnfainducedendothelialdysfunctionthroughmir21mediatedddah1admanosignalpathway AT tanshenglan dihydromyricetinattenuatestnfainducedendothelialdysfunctionthroughmir21mediatedddah1admanosignalpathway AT yangzhousheng dihydromyricetinattenuatestnfainducedendothelialdysfunctionthroughmir21mediatedddah1admanosignalpathway AT jiangpei dihydromyricetinattenuatestnfainducedendothelialdysfunctionthroughmir21mediatedddah1admanosignalpathway AT qincaie dihydromyricetinattenuatestnfainducedendothelialdysfunctionthroughmir21mediatedddah1admanosignalpathway AT yuanqiong dihydromyricetinattenuatestnfainducedendothelialdysfunctionthroughmir21mediatedddah1admanosignalpathway AT dangruili dihydromyricetinattenuatestnfainducedendothelialdysfunctionthroughmir21mediatedddah1admanosignalpathway AT yaoxiaoxia dihydromyricetinattenuatestnfainducedendothelialdysfunctionthroughmir21mediatedddah1admanosignalpathway AT qujian dihydromyricetinattenuatestnfainducedendothelialdysfunctionthroughmir21mediatedddah1admanosignalpathway AT luqiong dihydromyricetinattenuatestnfainducedendothelialdysfunctionthroughmir21mediatedddah1admanosignalpathway AT xuping dihydromyricetinattenuatestnfainducedendothelialdysfunctionthroughmir21mediatedddah1admanosignalpathway AT zhangbikui dihydromyricetinattenuatestnfainducedendothelialdysfunctionthroughmir21mediatedddah1admanosignalpathway AT xiangdaxiong dihydromyricetinattenuatestnfainducedendothelialdysfunctionthroughmir21mediatedddah1admanosignalpathway AT chenlei dihydromyricetinattenuatestnfainducedendothelialdysfunctionthroughmir21mediatedddah1admanosignalpathway |