دورية أكاديمية
Tetrahydroxystilbene Glucoside Protects Against Oxidized LDL-Induced Endothelial Dysfunction via Regulating Vimentin Cytoskeleton and its Colocalization with ICAM-1 and VCAM-1
| العنوان: | Tetrahydroxystilbene Glucoside Protects Against Oxidized LDL-Induced Endothelial Dysfunction via Regulating Vimentin Cytoskeleton and its Colocalization with ICAM-1 and VCAM-1 |
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| المؤلفون: | Wenjuan Yao, Chao Huang, Qinju Sun, Xiang Jing, Huiming Wang, Wei Zhang |
| المصدر: | Cellular Physiology and Biochemistry, Vol 34, Iss 5, Pp 1442-1454 (2014) |
| بيانات النشر: | Cell Physiol Biochem Press GmbH & Co KG, 2014. |
| سنة النشر: | 2014 |
| المجموعة: | LCC:Physiology LCC:Biochemistry |
| مصطلحات موضوعية: | Tetrahydroxystilbene glucoside, Oxidized LDL, Endothelial dysfunction, Vimentin, Physiology, QP1-981, Biochemistry, QD415-436 |
| الوصف: | Background: Endothelial cell dysfunction triggered by oxidized low-density lipoprotein (oxLDL) is the main event occurring during the development of atherosclerosis. 2,3,5,4'-tetrahydroxystilbene-2-O-β-D-glucoside (TSG), an active component of the rhizome extract from Polygonum multiflorum, exhibits significant anti-atherosclerotic activity. However, the protective effects of TSG against oxLDL-induced endothelial dysfunction have not been clarified. We investigated the cytoprotective effects of TSG in human umbilical vein endothelial cells (HUVECs) and explored underlying mechanisms. Methods and Results: TSG pretreatment markedly attenuated oxLDL-mediated loss of cell viability, release of lactate dehydrogenase (LDH), cell apoptosis, and monocyte adhesion. OxLDL increased vimentin mRNA and protein levels, vimentin cleavage, caspase-3 activation, adhesion molecules levels and their colocalization with vimentin in HUVECs. These alterations were attenuated by pretreatment with TSG. Meanwhile, TSG inhibited both the expression of TGFβ1 and the phosphorylation of Smad2 and Smad3, and TSG suppressed the nuclear translocation of Smad4 induced by oxLDL. Using shRNA, oxLDL-induced cell apoptosis and monocyte adhesion were significantly inhibited by vimentin suppression in HUVECs. Conclusions: These results suggest that TSG protects HUVECs against oxLDL-induced endothelial dysfunction through inhibiting vimentin expression and cleavage, and the expression of adhesion molecules and their colocalization with vimentin. The interruption of TGFβ/Smad pathway and caspase-3 activation appears to be responsible for the downregulation of TSG on vimentin expression and fragmentation, respectively. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 1015-8987 1421-9778 |
| Relation: | http://www.karger.com/Article/FullText/366349; https://doaj.org/toc/1015-8987; https://doaj.org/toc/1421-9778 |
| DOI: | 10.1159/000366349 |
| URL الوصول: | https://doaj.org/article/87d112ef7442454cb850e6ce8420f2ff |
| رقم الأكسشن: | edsdoj.87d112ef7442454cb850e6ce8420f2ff |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 10158987 14219778 |
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| DOI: | 10.1159/000366349 |