Endoglin is not expressed with cell adhesion molecules in aorta during atherogenesis in apoE-deficient mice
Jazyk angličtina Země Španělsko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
25208891
DOI
10.14670/hh-30.233
PII: HH-11-537
Knihovny.cz E-zdroje
- MeSH
- aorta metabolismus MeSH
- apolipoproteiny E nedostatek genetika MeSH
- aterosklerotický plát patologie MeSH
- ateroskleróza genetika MeSH
- cévní buněčněadhezivní molekula-1 biosyntéza MeSH
- dieta aterogenní MeSH
- endoglin MeSH
- intracelulární signální peptidy a proteiny biosyntéza MeSH
- lipidy krev MeSH
- makrofágy metabolismus MeSH
- molekuly buněčné adheze biosyntéza MeSH
- myši inbrední C57BL MeSH
- myši MeSH
- P-selektin biosyntéza MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- apolipoproteiny E MeSH
- cévní buněčněadhezivní molekula-1 MeSH
- endoglin MeSH
- Eng protein, mouse MeSH Prohlížeč
- intracelulární signální peptidy a proteiny MeSH
- lipidy MeSH
- molekuly buněčné adheze MeSH
- P-selektin MeSH
Endoglin (TGF-β receptor III), has been demonstrated to affect vascular endothelium and atherosclerosis. Moreover, it was also demonstrated that endoglin is involved in inflammation and plays a role in leukocyte adhesion and transmigration in vitro and in vivo but not in atherosclerosis related vessels. In this study, we wanted to evaluate endoglin expression in two different parts of the aorta (heart aortic sinus and ascending aorta) and assess its potential simultaneous expression with cell adhesion molecules in non-atherosclerotic and atherosclerotic aortas of apoE-deficient mice. Ten-week-old female apolipoprotein E-deficient mice on a C57BL/6J background (n=24) were randomly subdivided into three groups and were fed either chow diet (for another two months) or Western type diet (for another two or four months). Immunohistochemical staining of endoglin, VCAM-1 and P-selectin in aortic sinus and ascending aorta was performed. Endoglin expression was detected only in endothelial cells and varied during atherogenic process in aorta but not in aortic sinus. Moreover, its expression seemed to be weaker in aorta when compared to aortic sinus and the positivity was detected only in endothelium covering atherosclerotic lesions but not in non-atherosclerotic endothelium regardless of the plaque size. Endoglin was not expressed with P selectin and VCAM-1 in aortic endothelium in any studied group. This study shows that endothelial expression of endoglin is related to the atherogenic process predominantly in aorta outside the heart. Moreover, endoglin is not localized with cell adhesion molecules involved in atherosclerosis, suggesting it might not participate in leukocyte accumulation in aorta of apoE-deficient mice during atherogenesis.
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