ArticleCell adhesion & migration
NHE-1 and β1 integrin dependent monocyte adhesion and migration after glucose, insulin or PPARγ stimulation.
Article in Cell adhesion & migration. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- Soluble TGFBI aggravates the malignancy of cholangiocarcinoma through activation of the ITGB1 dependent PPARγ signalling pathway.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Reduction of endoglin receptor impairs mononuclear cell-migration.Exploration of medicine · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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Abstract
In the present study the effect of high glucose concentrations, insulin, PPARγ activators (rosiglitazone) and NHE-1 inhibitors (cariporide) in atherosclerosis-related functions of human monocytes was investigated. Monocyte adhesion to laminin-1, collagen type IV and endothelial cells, as well as monocyte migration through the same substrates were studied. Incubation of the monocyte suspension with high glucose concentrations, insulin and rosiglitazone induced all the studied atherosclerosis-related functions of the monocytes. In all these functions the addition of cariporide counteracted the activity of glucose, insulin and rosiglitazone. The use of antigen for β1 integrin also counteracted the activity of the above in monocyte adhesion in all three substrates. The data of the present study suggests that PPARγ activation in monocytes induces atherosclerosis, and that NHE-1 and β1 integrin play an important role in the beginning of atherosclerosis.
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Registered trials
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