ArticleAtherosclerosis2018
Elevated circulating TGF-β is not the cause of increased atherosclerosis development in biglycan deficient mice.
Article in Atherosclerosis, 2018. 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.
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Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- Biglycan: an emerging small leucine-rich proteoglycan (SLRP) marker and its clinicopathological significance.Molecular and cellular biochemistry · 2021Review
- Transforming Growth Factor Beta Receptor 3 Haplotypes in Sickle Cell Disease Are Associated with Lipid Profile and Clinical Manifestations.Mediators of inflammation · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND AND
aimsVascular biglycan contributes to atherosclerosis development and increased biglycan expression correlates with increased atherosclerosis. However, mice deficient in biglycan have either no reduction in atherosclerosis or an unexpected increase in atherosclerosis. Biglycan deficient mice have systemically elevated TGF-β, likely due to lack of sequestration of TGF-β in the extracellular matrix. The purpose of this study was to determine if prevention of TGF-β elevations in biglycan deficient mice affected atherosclerosis development.
methodsBiglycan deficient mice were crossed to Ldlr deficient mice. Diabetes was induced via streptozotocin and all mice were fed a high cholesterol diet. Diabetic biglycan wild type and biglycan deficient Ldlr deficient mice were injected with the TGF-β neutralizing antibody 1D11 or the irrelevant control antibody 13C4.
resultsBiglycan deficient mice had significantly elevated plasma TGF-β levels, which was further increased by diabetes, and significantly increased atherosclerosis. There was a significant correlation between TGF-β concentrations and atherosclerosis. However, despite nearly complete suppression of plasma TGF-β levels in mice treated with the TGF-β neutralizing antibody 1D11, there was no significant difference in atherosclerosis between mice with elevated TGF-β levels and mice with suppressed TGF-β levels.
conclusionsThe increased atherosclerosis in biglycan deficient mice does not appear to be due to elevations in TGF-β.
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Registered trials
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