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: | Chao Huang, Xiang Jing, Wenjuan Yao, Huiming Wang, Qinju Sun, Wei Zhang |
| المصدر: | Cellular Physiology and Biochemistry, Vol 34, Iss 5, Pp 1442-1454 (2014) |
| بيانات النشر: | S. Karger AG, 2014. |
| سنة النشر: | 2014 |
| مصطلحات موضوعية: | Oxidized LDL, Physiology, Down-Regulation, Vascular Cell Adhesion Molecule-1, Apoptosis, Vimentin, Protective Agents, lcsh:Physiology, lcsh:Biochemistry, chemistry.chemical_compound, Glucosides, Stilbenes, Human Umbilical Vein Endothelial Cells, medicine, Humans, lcsh:QD415-436, Endothelial dysfunction, VCAM-1, Cells, Cultured, Cytoskeleton, Tetrahydroxystilbene glucoside, ICAM-1, lcsh:QP1-981, biology, Caspase 3, Cell adhesion molecule, NF-kappa B, Endothelial Cells, Colocalization, Atherosclerosis, Intercellular Adhesion Molecule-1, medicine.disease, Smad Proteins, Receptor-Regulated, Cell biology, Lipoproteins, LDL, Endothelial stem cell, Biochemistry, chemistry, biology.protein, lipids (amino acids, peptides, and proteins), Signal Transduction |
| 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. |
| تدمد: | 1421-9778 1015-8987 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4b8be7bb4a7fd32438313df6c94b357a https://doi.org/10.1159/000366349 |
| حقوق: | OPEN |
| رقم الأكسشن: | edsair.doi.dedup.....4b8be7bb4a7fd32438313df6c94b357a |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 14219778 10158987 |
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