Endoglin as a possible marker of atorvastatin treatment benefit in atherosclerosis
Language English Country Netherlands Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
21440631
DOI
10.1016/j.phrs.2011.03.008
PII: S1043-6618(11)00072-7
Knihovny.cz E-resources
- MeSH
- Activin Receptors, Type I metabolism MeSH
- Activin Receptors, Type II MeSH
- Apolipoproteins E genetics MeSH
- Plaque, Atherosclerotic chemically induced metabolism pathology prevention & control MeSH
- Atherosclerosis blood chemically induced metabolism pathology prevention & control MeSH
- Atorvastatin MeSH
- Biomarkers, Pharmacological blood metabolism MeSH
- Cholesterol, Dietary pharmacology MeSH
- Cholesterol blood MeSH
- Endoglin MeSH
- Phosphorylation drug effects MeSH
- Cholesterol, HDL blood MeSH
- Intracellular Signaling Peptides and Proteins blood metabolism MeSH
- Blood drug effects MeSH
- Heptanoic Acids pharmacology therapeutic use MeSH
- Cholesterol, LDL blood MeSH
- Mice, Inbred C57BL MeSH
- Mice, Knockout MeSH
- Mice MeSH
- Smad1 Protein metabolism MeSH
- Pyrroles pharmacology therapeutic use MeSH
- Receptors, LDL genetics MeSH
- Sinus of Valsalva metabolism pathology MeSH
- Vascular Endothelial Growth Factor A metabolism MeSH
- Cholesterol, VLDL blood MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Acvrl1 protein, mouse MeSH Browser
- Activin Receptors, Type I MeSH
- Activin Receptors, Type II MeSH
- Apolipoproteins E MeSH
- Atorvastatin MeSH
- Biomarkers, Pharmacological MeSH
- Cholesterol, Dietary MeSH
- Cholesterol MeSH
- Endoglin MeSH
- Eng protein, mouse MeSH Browser
- Cholesterol, HDL MeSH
- Intracellular Signaling Peptides and Proteins MeSH
- Heptanoic Acids MeSH
- Cholesterol, LDL MeSH
- Smad1 Protein MeSH
- Pyrroles MeSH
- Receptors, LDL MeSH
- Smad1 protein, mouse MeSH Browser
- vascular endothelial growth factor A, mouse MeSH Browser
- Vascular Endothelial Growth Factor A MeSH
- Cholesterol, VLDL MeSH
Endoglin (a type III TGF-β receptor) is able to modulate ligand binding and signaling by association with the TGF-β type I receptors (ALK-1 and ALK-5). In this study, we hypothesized whether atorvastatin treatment affects endoglin/ALK-1/p-Smad1/VEGF expression in the aorta and endoglin levels in serum in ApoE/LDLR double knockout mice. ApoE/LDLR double knockout mice were fed with a diet containing either 1% of cholesterol (CHOL) or cholesterol with atorvastatin (ATV) at a dose of 50mg/kg/day. Biochemical analysis of cholesterol levels and ELISA analysis of endoglin levels in serum, lesion area size, immunohistochemistry and Western blot analysis in mice aorta were performed. Atorvastatin treatment resulted in a significant decrease of total, VLDL and LDL cholesterol, atherosclerotic lesion size and endoglin serum levels in comparison with CHOL mice. On the other hand, atorvastatin treatment significantly increased the expressions of endoglin by 1431%, ALK-1 by 310%, p-Smad1 by 135% and VEGF by 62% in aorta when compared to CHOL mice. In conclusion, it has been demonstrated that atorvastatin increases endoglin/ALK-1/p-Smad1/VEGF expression in aorta and decreases the size of atherosclerotic lesions, suggesting that activation of this endothelial-protective pathway might support the antiatherogenic effects of atorvastatin. Moreover, atorvastatin concurrently decreased serum levels of endoglin suggesting that monitoring of endoglin levels in blood might represent an important marker of the progression and/or treatment of atherosclerosis.
References provided by Crossref.org
High soluble endoglin levels do not induce endothelial dysfunction in mouse aorta
