Soluble endoglin and hypercholesterolemia aggravate endothelial and vessel wall dysfunction in mouse aorta

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11160%2F18%3A10382084" target="_blank" >RIV/00216208:11160/18:10382084 - isvavai.cz</a>

Alternative codes found

RIV/00179906:_____/18:10382084

Result on the web

<a href="http://www.sciencedirect.com/science/article/pii/S0021915018300674" target="_blank" >http://www.sciencedirect.com/science/article/pii/S0021915018300674</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.atherosclerosis.2018.02.008" target="_blank" >10.1016/j.atherosclerosis.2018.02.008</a>

Result language

angličtina

Original language name

Soluble endoglin and hypercholesterolemia aggravate endothelial and vessel wall dysfunction in mouse aorta

Original language description

Background and aims: Increased plasma levels of soluble endoglin (sEng) were detected in patients with endothelial dysfunction-related disorders and hypercholesterolemia. In this study, we hypothesized that high levels of sEng accompanied by mild hypercholesterolemia could aggravate endothelial and vessel wall dysfunction and affect endoglin/eNOS signaling in mouse aorta. Methods: Three-month-old female transgenic mice on CBAxC57BL/6J background, with high levels of sEng (Sol-Eng(+) high HFD), and their littermates with low levels of sEng (Sol-Eng(+) low HFD), were fed a high fat diet for six months. Plasma samples were used for biochemical, ELISA and Luminex analyses of total cholesterol, sEng and inflammatory markers. Functional parameters of aorta were assessed with wire myograph 620M. Western blot analyses of membrane endoglin/eNOS signaling and endothelial dysfunction/inflammation markers in aorta were performed. Results: Functional analysis of aorta showed impaired KCl induced vasoconstriction, endothelial-dependent relaxation after the administration of acetylcholine as well as endothelial-independent relaxation induced by sodium nitroprusside in the Sol-Eng(+) high HFD group compared to the Sol-Eng(+) low HFD group. Ach-induced vasodilation after administration of L-NAME was significantly higher in the Sol-Eng(+) high HFD group compared to the Sol-Eng(+) low HFD group. The expression of endoglin, p-eNOS/eNOS, pSmad2/3/Smad2/3 signaling pathway was significantly lower in the Sol-Eng(+) high HFD group compared to the Sol-Eng(+) low HFD group. Conclusions: The results indicate that long-term hypercholesterolemia combined with high levels of sEng leads to the aggravation of endothelial and vessel wall dysfunction in aorta, with possible alterations of the membrane endoglin/eNOS signaling, suggesting that high levels of soluble endoglin might be considered as a risk factor of cardiovascular diseases.

Czech name

—

Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

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OECD FORD branch

30104 - Pharmacology and pharmacy

Project

Result was created during the realization of more than one project. More information in the Projects tab.

Continuities

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Publication year

2018

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Atherosclerosis

ISSN

0021-9150

e-ISSN

—

Volume of the periodical

271

Issue of the periodical within the volume

April

Country of publishing house

IE - IRELAND

Number of pages

11

Pages from-to

15-25

UT code for WoS article

000428090400003

EID of the result in the Scopus database

2-s2.0-85042232760