ArticleEndocrine2009
Ablation of NF-kappaB expression by small interference RNA prevents the dysfunction of human umbilical vein endothelial cells induced by high glucose.
Article in Endocrine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 14 citations in OpenAlex.
- High glucose-induced hyperosmolarity contributes to COX-2 expression and angiogenesis: implications for diabetic retinopathy.Cardiovascular diabetology · 2016Article
- Resveratrol protects vascular endothelial cells from high glucose-induced apoptosis through inhibition of NADPH oxidase activation-driven oxidative stress.CNS neuroscience & therapeutics · 2013Article
- The effect of NF-κB pathway on proliferation and apoptosis of human umbilical vein endothelial cells induced by intermittent high glucose.Molecular and cellular biochemistry · 2011Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes is a major independent risk factor for cardiovascular disease and stroke. High glucose (HG) reduces endothelial cell (EC) proliferation with a concomitant increase in apoptosis. HG also induces the translocation of nuclear factor (NF)-kappaB in human umbilical vein endothelial cells (HUVECs). However, data regarding the relationship between NF-kappaB signaling and HG-induced endothelial dysfunction are limited. In the present study, we constructed an NF-kappaB-targeting RNA interference (RNAi) adenovirus vector and cultured HUVECs in 5.5, 20.5, or 30.5 mM D: -glucose or in daily alternating 5.5 or 30.5 mM D: -glucose. We assessed the effects of the NF-kappaB pathway on proliferation under HG conditions by measuring bromodeoxyuridine incorporation and conducting methyl thiazolyltetrazolium assays. We also tested apoptosis by performing flow cytometry and terminal deoxynucleotidyl transferase nick-end labeling assay. The RNAi adenovirus effectively downregulated expression of the p65 protein in HUVECs for more than 6 days. Blockage of the NF-kappaB pathway with the RNAi adenovirus substantially protected HUVECs from decreased proliferation and reduced cellular apoptosis in HG conditions. These findings may explain how hyperglycemia promotes dysfunction of ECs and could elucidate a potential new target for therapeutic interventions.
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Registered trials
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