ArticleJournal of cellular and molecular medicine2019
Trans-repression of NFκB pathway mediated by PPARγ improves vascular endothelium insulin resistance.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Preventive Effect of Oleanolic Acid on Ulcerative Colitis Caused by Dextran Sulfate Sodium via a PPARγ-Involved Mechanism in Mice.Drug design, development and therapy · 2025Article
- Therapeutic Targeting of PPARγ in Nonalcoholic Fatty Liver Disease: Efficacy, Safety, and Drug Development.Drug design, development and therapy · 2025Review
- Effect of temperature-sensitive nanogel combined with angioplasty on sICAM-1 and VE-cadherin in lower extremity arterial occlusion rabbits.Bioengineered · 2021Article
- Diabetes pathogenesis and management: the endothelium comes of age.Journal of molecular cell biology · 2021Article
- MiR-3138 deteriorates the insulin resistance of HUVECs via KSR2/AMPK/GLUT4 signaling pathway.Cell cycle (Georgetown, Tex.) · 2021Article
- Ginsenoside Rc Ameliorates Endothelial Insulin Resistance via Upregulation of Angiotensin-Converting Enzyme 2.Frontiers in pharmacology · 2021Article
- Trans-repression of NFκB pathway mediated by PPARγ improves vascular endothelium insulin resistance.Journal of cellular and molecular medicine · 2019Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous study has shown that thiazolidinediones (TZDs) improved endothelium insulin resistance (IR) induced by high glucose concentration (HG)/hyperglycaemia through a PPARγ-dependent-NFκB trans-repression mechanism. However, it is unclear, whether changes in PPARγ expression affect the endothelium IR and what the underlying mechanism is. In the present study, we aimed to address this issue. HG-treated human umbilical vascular endothelial cells (HUVEC) were transfected by either PPARγ-overexpressing (Ad-PPARγ) or PPARγ-shRNA-containing (Ad-PPARγ-shRNA) adenoviral vectors. Likewise, the rats fed by high-fat diet (HFD) were infected by intravenous administration of Ad-PPARγ or Ad-PPARγ-shRNA. The levels of nitric oxide (NO), endothelin-1 (ET-1) and cytokines (TNFα, IL-6, sICAM-1 and sVCAM-1) and the expression levels of PPARγ, eNOS, AKT, p-AKT, IKKα/β and p-IKKα/β and IκBα were examined; and the interaction between PPARγ and NFκB-P65 as well as vascular function were evaluated. Our present results showed that overexpression of PPARγ notably increased the levels of NO, eNOS, p-AKT and IκBα as well as the interaction of PPARγ and NFκB-P65, and decreased the levels of ET-1, p-IKKα/β, TNFα, IL-6, sICAM-1 and sVCAM-1. In contrast, down-expression of PPARγ displayed the opposite effects. The results demonstrate that the overexpression of PPARγ improves while the down-expression worsens the endothelium IR via a PPARγ-mediated NFκB trans-repression dependent manner. The findings suggest PPARγ is a potential therapeutic target for diabetic vascular complications.
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