ArticleBiochemical and biophysical research communications2009
4-HNE inhibits tube formation and up-regulates chondromodulin-I in human endothelial cells.
Article in Biochemical and biophysical research communications, 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, 10 citations in OpenAlex.
- The Potential Role of Mitochondrial Acetaldehyde Dehydrogenase 2 in Urological Cancers From the Perspective of Ferroptosis and Cellular Senescence.Frontiers in cell and developmental biology · 2022Review
- 4-Hydroxynonenal Contributes to Angiogenesis through a Redox-Dependent Sphingolipid Pathway: Prevention by Hydralazine Derivatives.Oxidative medicine and cellular longevity · 2017Article
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The aim of the present study was to investigate the effects of 4-hydroxy-2-nonenal (4-HNE) on tube formation by human bone marrow endothelial cells (HBMEC). We found that 4-HNE at physiologically achievable concentrations (5 and 10 microM) inhibited the formation of tubes. Western blot analysis revealed that inhibition of tube formation by 4-HNE was associated with increased expression of chondromodulin-I (CHM-I), a protein with well-known anti-angiogenic properties. Cell viability assays showed that 4-HNE at concentrations of 10 microM or less did not cause HBMEC cell death. Luciferase reporter assays did not show any inducing effect of 4-HNE on the promoter activity of human CHM-I gene indicating that post-transcriptional or post-translational modifications may account for the up-regulation of CHM-I. Collectively, the results of the present study show for the first time that 4-HNE inhibits tube formation by HBMECs indicating a potential anti-angiogenic activity of 4-HNE. This inhibition occurs at least in part via 4-HNE-induced CHM-I protein expression.
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Registered trials
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