Cholesterol effects on endoglin and its downstream pathways in ApoE/LDLR double knockout mice
Jazyk angličtina Země Japonsko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
21576826
DOI
10.1253/circj.cj-10-1285
PII: JST.JSTAGE/circj/CJ-10-1285
Knihovny.cz E-zdroje
- MeSH
- aktivinové receptory typu I metabolismus MeSH
- aktivinové receptory typu II MeSH
- aktivinové receptory metabolismus MeSH
- aorta metabolismus patologie MeSH
- apolipoproteiny E nedostatek genetika metabolismus MeSH
- aterosklerotický plát metabolismus patologie MeSH
- ateroskleróza metabolismus patologie MeSH
- biologické markery krev MeSH
- cholesterol dietní farmakologie MeSH
- cholesterol krev MeSH
- endoglin MeSH
- intracelulární signální peptidy a proteiny krev MeSH
- modely nemocí na zvířatech MeSH
- myši knockoutované MeSH
- myši MeSH
- protein Smad1 metabolismus MeSH
- protein Smad2 metabolismus MeSH
- protein-serin-threoninkinasy metabolismus MeSH
- receptory LDL nedostatek genetika metabolismus MeSH
- receptory transformujícího růstového faktoru beta metabolismus MeSH
- signální transdukce účinky léků fyziologie MeSH
- synthasa oxidu dusnatého, typ III metabolismus MeSH
- TGF-beta receptor I. typu MeSH
- vaskulární endoteliální růstový faktor A metabolismus MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- Acvrl1 protein, mouse MeSH Prohlížeč
- aktivinové receptory typu I MeSH
- aktivinové receptory typu II MeSH
- aktivinové receptory MeSH
- apolipoproteiny E MeSH
- biologické markery MeSH
- cholesterol dietní MeSH
- cholesterol MeSH
- endoglin MeSH
- Eng protein, mouse MeSH Prohlížeč
- intracelulární signální peptidy a proteiny MeSH
- protein Smad1 MeSH
- protein Smad2 MeSH
- protein-serin-threoninkinasy MeSH
- receptory LDL MeSH
- receptory transformujícího růstového faktoru beta MeSH
- Smad1 protein, mouse MeSH Prohlížeč
- Smad2 protein, mouse MeSH Prohlížeč
- synthasa oxidu dusnatého, typ III MeSH
- TGF-beta receptor I. typu MeSH
- Tgfbr1 protein, mouse MeSH Prohlížeč
- vaskulární endoteliální růstový faktor A MeSH
BACKGROUND: The aim of the study was to evaluate whether cholesterol-rich diet affects transforming growth factor-β-RIII (endoglin) levels in blood and 2 endoglin-related pathways in the aorta of ApoE/LDLR double knockout mice. METHODS AND RESULTS: Mice were fed either chow diet (CHOW) (n=8) or by 1% cholesterol-rich diet (CHOL) (n=8). Biochemical analysis of cholesterol and endoglin levels in blood, lesion size area, immunohistochemistry and Western blot analysis in mice aortas were performed. Biochemical analysis showed that cholesterol-rich diet resulted in a significant increase of cholesterol and endoglin levels in serum, and increased plaque size in the aorta. In addition, a cholesterol-rich diet significantly decreased the expressions of endoglin by 92%, activin receptor-like kinase (ALK)-1 by 71%, p-Smad2 by 21%, and vascular endothelial growth factor (VEGF) by 37% when compared to CHOW mice, but ALK-5, p-Smad1, and endothelial nitric oxide synthase were not significantly affected. CONCLUSIONS: Hypercholesterolemia increases endoglin levels in blood and simultaneously decreases its expression in aorta, together with atherosclerosis protective markers p-Smad2 and VEGF, followed by increased plaque size. Inhibition of endoglin signaling might be one of the mechanisms responsible for the promoting of endothelial dysfunction and atherogenesis. Moreover, the monitoring of endoglin serum levels might represent an attractive blood marker of progression of disease; however, the precise source and role of endoglin in blood serum remains to be elucidated.
Citace poskytuje Crossref.org
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