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

Kód výsledku v 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>

Nalezeny alternativní kódy

RIV/00216208:11160/17:10365232

Výsledek na webu

<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>

Jazyk výsledku

angličtina

Název v původním jazyce

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

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

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

Popis výsledku anglicky

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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30104 - Pharmacology and pharmacy

Projekt

<a href="/cs/project/GA15-24015S" target="_blank" >GA15-24015S: Tkáňový a solubilní endoglin a jejich význam v endoteliální dysfunkci a aterogenezi in vivo a in vitro</a><br>

Návaznosti

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

Rok uplatnění

2017

Kód důvěrnosti údajů

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

Název periodika

Life Sciences

ISSN

0024-3205

e-ISSN

—

Svazek periodika

175

Číslo periodika v rámci svazku

April

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

9

Strana od-do

52-60

Kód UT WoS článku

000400537800008

EID výsledku v databázi Scopus

2-s2.0-85016392365