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Statements

Subject Item
n2:RIV%2F00216208%3A11160%2F12%3A10124865%21RIV13-MSM-11160___
rdf:type
n6:Vysledek skos:Concept
rdfs:seeAlso
http://www.sciencedirect.com/science/article/pii/S002191501200158X
dcterms:description
Endoglin (CD 105, TGF-beta receptor III) is a homodimeric transmembrane glycoprotein that plays a regulatory role in TGF-beta signaling. Its functional role in the context of atherosclerosis has yet to be defined and should be stated here. Therefore, we focused on the role of endoglin in atherosclerosis in both humans and experimental animals. Endoglin expression was demonstrated in atherosclerotic vessels predominantly in endothelial cells and smooth muscle cells in various types of blood vessels in mice and humans, suggesting its participation in atherogenesis. Endoglin expression was also related to the expression of eNOS in endothelium, repair of the vessel wall, plaque neoangiogenesis, production of collagen and stabilization of atherosclerotic lesions. In addition, increased levels of soluble endoglin were associated with hypercholesterolemia, atherosclerosis, acute myocardial infarction and were related to inhibition of TGF-beta signaling in the vessel wall. Moreover, soluble endoglin levels were significantly lowered after a series of extracorporeal eliminations in patients with familial hypercholesterolemia. Additionally, statin treatment decreased levels of soluble endoglin and increased its expression in aorta, which was related to reduced atherosclerosis in mice. In conclusion, we propose that measurement of soluble endoglin might give information about progression of the atherosclerotic process or the efficacy of therapeutic interventions, which is the task that must be answered in clinical trials. Endoglin (CD 105, TGF-beta receptor III) is a homodimeric transmembrane glycoprotein that plays a regulatory role in TGF-beta signaling. Its functional role in the context of atherosclerosis has yet to be defined and should be stated here. Therefore, we focused on the role of endoglin in atherosclerosis in both humans and experimental animals. Endoglin expression was demonstrated in atherosclerotic vessels predominantly in endothelial cells and smooth muscle cells in various types of blood vessels in mice and humans, suggesting its participation in atherogenesis. Endoglin expression was also related to the expression of eNOS in endothelium, repair of the vessel wall, plaque neoangiogenesis, production of collagen and stabilization of atherosclerotic lesions. In addition, increased levels of soluble endoglin were associated with hypercholesterolemia, atherosclerosis, acute myocardial infarction and were related to inhibition of TGF-beta signaling in the vessel wall. Moreover, soluble endoglin levels were significantly lowered after a series of extracorporeal eliminations in patients with familial hypercholesterolemia. Additionally, statin treatment decreased levels of soluble endoglin and increased its expression in aorta, which was related to reduced atherosclerosis in mice. In conclusion, we propose that measurement of soluble endoglin might give information about progression of the atherosclerotic process or the efficacy of therapeutic interventions, which is the task that must be answered in clinical trials.
dcterms:title
The role of endoglin in atherosclerosis The role of endoglin in atherosclerosis
skos:prefLabel
The role of endoglin in atherosclerosis The role of endoglin in atherosclerosis
skos:notation
RIV/00216208:11160/12:10124865!RIV13-MSM-11160___
n6:predkladatel
n18:orjk%3A11160
n3:aktivita
n14:I n14:S
n3:aktivity
I, S
n3:cisloPeriodika
1
n3:dodaniDat
n7:2013
n3:domaciTvurceVysledku
n9:4345967 n9:5780462 n9:9316779 n9:4987438
n3:druhVysledku
n19:J
n3:duvernostUdaju
n12:S
n3:entitaPredkladatele
n11:predkladatel
n3:idSjednocenehoVysledku
165995
n3:idVysledku
RIV/00216208:11160/12:10124865
n3:jazykVysledku
n17:eng
n3:klicovaSlova
TGF-beta 1 signaling; Statins; Cholesterol; Atherosclerosis; Endoglin
n3:klicoveSlovo
n5:Atherosclerosis n5:Statins n5:Endoglin n5:Cholesterol n5:TGF-beta%201%20signaling
n3:kodStatuVydavatele
NL - Nizozemsko
n3:kontrolniKodProRIV
[C0E9700A4D08]
n3:nazevZdroje
Atherosclerosis
n3:obor
n15:FA
n3:pocetDomacichTvurcuVysledku
4
n3:pocetTvurcuVysledku
4
n3:rokUplatneniVysledku
n7:2012
n3:svazekPeriodika
224
n3:tvurceVysledku
Zemánková, Lenka Nachtigal, Petr Stráský, Zbyněk Rathouská, Jana
n3:wos
000308078000002
s:issn
0021-9150
s:numberOfPages
8
n8:doi
10.1016/j.atherosclerosis.2012.03.001
n20:organizacniJednotka
11160