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Soluble Endoglin as a Potential Biomarker of Nonalcoholic Steatohepatitis (NASH) Development, Participating in Aggravation of NASH-Related Changes in Mouse Liver
IC. Igreja Sá, K. Tripska, M. Hroch, R. Hyspler, A. Ticha, H. Lastuvkova, J. Schreiberova, E. Dolezelova, S. Eissazadeh, B. Vitverova, I. Najmanova, M. Vasinova, M. Pericacho, S. Micuda, P. Nachtigal
Jazyk angličtina Země Švýcarsko
Typ dokumentu časopisecké články
Grantová podpora
17-31754A
Ministerstvo Zdravotnictví Ceské Republiky
CZ.02.1.01/0.0/0.0/16_019/0000841
Univerzita Karlova v Praze
1166119
Grantová Agentura, Univerzita Karlova
SVV 260 549
Univerzita Karlova v Praze
NV17-31754A
MZ0
CEP - Centrální evidence projektů
Digitální knihovna NLK
Plný text - Článek
Free Medical Journals od 2000
Freely Accessible Science Journals od 2000
PubMed Central od 2007
Europe PubMed Central od 2007
ProQuest Central od 2000-03-01
Open Access Digital Library od 2000-01-01
Open Access Digital Library od 2007-01-01
Health & Medicine (ProQuest) od 2000-03-01
ROAD: Directory of Open Access Scholarly Resources od 2000
Odkazy
PubMed
33261044
DOI
10.3390/ijms21239021
Knihovny.cz E-zdroje
- MeSH
- alkalická fosfatasa metabolismus MeSH
- aspartátaminotransferasy metabolismus MeSH
- biologické markery krev metabolismus MeSH
- biologické modely MeSH
- cholesterol krev metabolismus MeSH
- dieta s vysokým obsahem tuků MeSH
- endoglin krev metabolismus MeSH
- fruktosa MeSH
- jaterní cirhóza krev komplikace patologie MeSH
- játra metabolismus patologie MeSH
- lidé MeSH
- modely nemocí na zvířatech MeSH
- myši MeSH
- nealkoholová steatóza jater krev komplikace metabolismus MeSH
- oxidační stres MeSH
- rozpustnost MeSH
- triglyceridy metabolismus MeSH
- zánět patologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
Nonalcoholic steatohepatitis (NASH) is characterized by hepatic steatosis with inflammation and fibrosis. Membrane endoglin (Eng) expression is shown to participate in fibrosis, and plasma concentrations of soluble endoglin (sEng) are increased in patients with hypercholesterolemia and type 2 diabetes mellitus. We hypothesize that NASH increases both hepatic Eng expression and sEng in blood and that high levels of sEng modulate cholesterol and bile acid (BA) metabolism and affect NASH progression. Three-month-old transgenic male mice overexpressing human sEng and their wild type littermates are fed for six months with either a high-saturated fat, high-fructose high-cholesterol (FFC) diet or a chow diet. Evaluation of NASH, Liquid chromatography-mass spectrometry (LC/MS) analysis of BA, hepatic expression of Eng, inflammation, fibrosis markers, enzymes and transporters involved in hepatic cholesterol and BA metabolism are assessed using Real-Time Quantitative Reverse Transcription Polymerase Chain reaction (qRT-PCR) and Western blot. The FFC diet significantly increases mouse sEng levels and increases hepatic expression of Eng. High levels of human sEng results in increased hepatic deposition of cholesterol due to reduced conversion into BA, as well as redirects the metabolism of triglycerides (TAG) to its accumulation in the liver, via reduced TAG elimination by β-oxidation combined with reduced hepatic efflux. We propose that sEng might be a biomarker of NASH development, and the presence of high levels of sEng might support NASH aggravation by impairing the essential defensive mechanism protecting NASH liver against excessive TAG and cholesterol accumulation, suggesting the importance of high sEng levels in patients prone to develop NASH.
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- $a Igreja Sá, Ivone Cristina $u Department of Biological and Medical Sciences, Faculty of Pharmacy in Hradec Kralove, Charles University, 500 05 Hradec Kralove, Czech Republic
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- $a Nonalcoholic steatohepatitis (NASH) is characterized by hepatic steatosis with inflammation and fibrosis. Membrane endoglin (Eng) expression is shown to participate in fibrosis, and plasma concentrations of soluble endoglin (sEng) are increased in patients with hypercholesterolemia and type 2 diabetes mellitus. We hypothesize that NASH increases both hepatic Eng expression and sEng in blood and that high levels of sEng modulate cholesterol and bile acid (BA) metabolism and affect NASH progression. Three-month-old transgenic male mice overexpressing human sEng and their wild type littermates are fed for six months with either a high-saturated fat, high-fructose high-cholesterol (FFC) diet or a chow diet. Evaluation of NASH, Liquid chromatography-mass spectrometry (LC/MS) analysis of BA, hepatic expression of Eng, inflammation, fibrosis markers, enzymes and transporters involved in hepatic cholesterol and BA metabolism are assessed using Real-Time Quantitative Reverse Transcription Polymerase Chain reaction (qRT-PCR) and Western blot. The FFC diet significantly increases mouse sEng levels and increases hepatic expression of Eng. High levels of human sEng results in increased hepatic deposition of cholesterol due to reduced conversion into BA, as well as redirects the metabolism of triglycerides (TAG) to its accumulation in the liver, via reduced TAG elimination by β-oxidation combined with reduced hepatic efflux. We propose that sEng might be a biomarker of NASH development, and the presence of high levels of sEng might support NASH aggravation by impairing the essential defensive mechanism protecting NASH liver against excessive TAG and cholesterol accumulation, suggesting the importance of high sEng levels in patients prone to develop NASH.
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