Soluble endoglin modulates the pro-inflammatory mediators NF-kappa B and IL-6 in cultured human endothelial cells

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11150%2F17%3A10365232" target="_blank" >RIV/00216208:11150/17:10365232 - isvavai.cz</a>

Alternative codes found

RIV/00216208:11160/17:10365232

Result on the web

<a href="http://www.sciencedirect.com/science/article/pii/S0024320517300978" target="_blank" >http://www.sciencedirect.com/science/article/pii/S0024320517300978</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.lfs.2017.03.014" target="_blank" >10.1016/j.lfs.2017.03.014</a>

Result language

angličtina

Original language name

Soluble endoglin modulates the pro-inflammatory mediators NF-kappa B and IL-6 in cultured human endothelial cells

Original language description

Aims: Endoglin is a transmembrane glycoprotein, that plays an important role in regulating endothelium. Proteolytic cleavage of membrane endoglin releases soluble endoglin (sEng), whose increased plasma levels have been detected in diseases related to the cardiovascular system. It was proposed that sEng might damage vascular endothelium, but detailed information about the potential mechanisms involved is not available. Thus, we hypothesized that sEng contributes to endothelial dysfunction, leading to a pro-inflammatory phenotype by a possible modulation of the TGF-beta and/or inflammatory pathways. Main methods: Human umbilical vein endothelial cells (HUVECs) and Human embryonic kidney cell line (HEK293T) were treated with different sEng concentration and time in order to reveal possible effect on biomarkers of inflammation and TGF-beta signaling. IL6 and NF kappa B reporter luciferase assays, quantitative real-time PCR analysis, Western blot analysis and immunofluorescence flow cytometry were used. Key findings: sEng treatment results in activation of NF-kappa B/IL-6 expression, increased expression of membrane endoglin and reduced expression of Id-1. On the other hand, no significant effects on other markers of endothelial dysfunction and inflammation, including eNOS, peNOS(S1177), VCAM-1, COX-1, COX-2 and ICAM-1 were detected. Significance: As a conclusion, sEng treatment resulted in an activation of NF-kappa B, IL-6, suggesting activation of pro inflammatory phenotype in endothelial cells. The precise mechanism of this activation and its consequence remains to be elucidated. A combined treatment of sEng with other cardiovascular risk factors will be necessary in order to reveal whether sEng is not only a biomarker of cardiovascular diseases, but also a protagonist of endothelial dysfunction.

Czech name

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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

—

OECD FORD branch

30104 - Pharmacology and pharmacy

Project

<a href="/en/project/GA15-24015S" target="_blank" >GA15-24015S: Tissue and soluble endoglin and their importance in endothelial dysfunction and atherogenesis in vivo and in vitro</a><br>

Continuities

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

Publication year

2017

Confidentiality

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

Name of the periodical

Life Sciences

ISSN

0024-3205

e-ISSN

—

Volume of the periodical

175

Issue of the periodical within the volume

April

Country of publishing house

GB - UNITED KINGDOM

Number of pages

9

Pages from-to

52-60

UT code for WoS article

000400537800008

EID of the result in the Scopus database

2-s2.0-85016392365