ArticleJournal of medical ultrasonics (2001)2015
Ultrasound up-regulates expression of heme oxygenase-1 gene in endothelial cells.
Article in Journal of medical ultrasonics (2001), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
1 citing paper in PubMed, 8 citations in OpenAlex.
- Ex Vivo Imaging of Ultrasound-Stimulated Metabolic Activity in Rat Pancreatic Slices.Ultrasound in medicine & biology · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeWe found heme oxygenase-1 (HO-1) gene up-regulation in response to ultrasound stimulation in endothelial cells. This project was started to explore the mechanism since it could be applied clinically.
methodsQuantitative real-time PCR experiments were conducted to determine the appropriate condition to up-regulate HO-1 gene expression. A promoter assay experiment and a microarray analysis were done to analyze signal transduction pathways to be activated in endothelial cells by ultrasound stimulation.
resultsApproximately, 33-fold up-regulation of HO-1 mRNA was observed when endothelial cells were exposed to 1-MHz ultrasound at 0.3 W/cm(2) and DF 10 % for 20 s. Data obtained from promoter analysis and microarray analysis suggested that the Nrf2/StRE signal pathway was involved in the up-regulation. In addition, ultrasound stimulation to endothelial cells changed its gene expression profile so that it could modify the anti-inflammatory, antioxidant, and vasodilatory activities in addition to pro-angiogenic and vascular reconstitution activities of endothelial cells.
conclusionIt was suggested that ultrasound stimulation of endothelial cells up-regulated HO-1 expression through intracellular oxidative stress, which subsequently changed the gene expression pattern so that it could modify vascular functions.
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Registered trials
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