Publications
Detailed Information
Rosiglitazone increases endothelial cell migration and vascular permeability through Akt phosphorylation
Cited 26 time in
Web of Science
Cited 28 time in Scopus
- Authors
- Issue Date
- 2017-08-30
- Publisher
- BioMed Central
- Citation
- BMC Pharmacology and Toxicology, 18(1):62
- Keywords
- Thiazolidinediones ; Rosiglitazone ; Endothelial cells ; Vascular permeability ; Edema ; Akt
- Abstract
- Abstract
Background
Thiazolidinediones (TZDs), peroxisome proliferator-activated receptor-γ (PPAR-γ) agonists, exhibit anti-inflammatory and antioxidant properties and inhibit endothelial inflammation and dysfunction, which is anti-atherogenic. However, fluid retention, which may lead to congestive heart failure and peripheral edema, is also a concern, which may result from endothelial cell leakage. In the current study, we examined the effects of PPAR-γ agonists on vascular endothelial cell migration and permeability in order to determine its underlying mechanisms.
Methods
We used rosiglitazone and conducted cell migration assay and permeability assay using HUVEC cells and measured vascular permeability and leakage in male C57BL/6 mice.
Results
Rosiglitazone significantly promoted endothelial cell migration and induced permeability via activation of phosphatidylinositol-3-kinase (PI3K) – Akt or protein kinase C (PKC)β. In addition, rosiglitazone increased vascular endothelial growth factor (VEGF) expression and suppressed expression of tight junction proteins (JAM-A and ZO-1), which might promote neovascularization and vascular leakage. These phenomena were reduced by Akt inhibition.
Conclusions
Vascular endothelial cell migration and permeability change through Akt phosphorylation might be a mechanism of induced fluid retention and peripheral tissue edema by TZD.
- ISSN
- 2050-6511
- Language
- English
- Files in This Item:
- Appears in Collections:
Item View & Download Count
Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.