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Statements

Subject Item
n2:RIV%2F61388963%3A_____%2F13%3A00394759%21RIV14-GA0-61388963
rdf:type
n4:Vysledek skos:Concept
dcterms:description
Both cardiovascular disease and liver injury are major public health issues. Hyperhomocysteinemia has been linked to cardiovascular diseases, and defects in methyl group metabolism, often resulting in hyperhomocysteinemia, are among the key molecular events postulated to play a role in liver injury. We employed proteomics and metabolomics analyses of human hepatocytes in primary cell culture to explore the spectrum of proteins and associated metabolites affected by the disruption of methyl group metabolism. We treated the hepatocytes with homocysteine (Hcy, 0.1 mM and 2 mM) to follow the impact of hyperhomocysteinemia, and in parallel, we used a specific inhibitor of betaine-homocysteine S-methyltransferase (BHMT) to extend our understanding of the physiological functions of the enzyme. The major effect of BHMT inhibition was a 50% decrease in S-adenosylmethionine levels. The treatments with Hcy resulted in multiple changes in the metabolite levels depending on the treatment modality. The BHMT inhibition and 0.1 mM Hcy treatment induced only moderate changes in the hepatocyte proteome and secretome, while the changes induced by the 2 mM Hcy treatment were extensive. Phosphatidylethanolamine carboxykinase and ornithine aminotransferase were up-regulated about two fold indicating an intervention into metabolism. Cellular proliferation was suspended, secretome composition was changed and signs of apoptosis were discernible. We have detected fibrinogen gamma dimers, which might have a role as a potentially new biomarker of early liver injury. Finally, we have demonstrated the failed maturation of apolipoprotein A1, which might be a new mechanism of disruption of cholesterol efflux from tissues. Both cardiovascular disease and liver injury are major public health issues. Hyperhomocysteinemia has been linked to cardiovascular diseases, and defects in methyl group metabolism, often resulting in hyperhomocysteinemia, are among the key molecular events postulated to play a role in liver injury. We employed proteomics and metabolomics analyses of human hepatocytes in primary cell culture to explore the spectrum of proteins and associated metabolites affected by the disruption of methyl group metabolism. We treated the hepatocytes with homocysteine (Hcy, 0.1 mM and 2 mM) to follow the impact of hyperhomocysteinemia, and in parallel, we used a specific inhibitor of betaine-homocysteine S-methyltransferase (BHMT) to extend our understanding of the physiological functions of the enzyme. The major effect of BHMT inhibition was a 50% decrease in S-adenosylmethionine levels. The treatments with Hcy resulted in multiple changes in the metabolite levels depending on the treatment modality. The BHMT inhibition and 0.1 mM Hcy treatment induced only moderate changes in the hepatocyte proteome and secretome, while the changes induced by the 2 mM Hcy treatment were extensive. Phosphatidylethanolamine carboxykinase and ornithine aminotransferase were up-regulated about two fold indicating an intervention into metabolism. Cellular proliferation was suspended, secretome composition was changed and signs of apoptosis were discernible. We have detected fibrinogen gamma dimers, which might have a role as a potentially new biomarker of early liver injury. Finally, we have demonstrated the failed maturation of apolipoprotein A1, which might be a new mechanism of disruption of cholesterol efflux from tissues.
dcterms:title
Effects of hyperhomocysteinemia and betaine-homocysteine S-methyltransferase inhibition on hepatocyte metabolites and the proteome Effects of hyperhomocysteinemia and betaine-homocysteine S-methyltransferase inhibition on hepatocyte metabolites and the proteome
skos:prefLabel
Effects of hyperhomocysteinemia and betaine-homocysteine S-methyltransferase inhibition on hepatocyte metabolites and the proteome Effects of hyperhomocysteinemia and betaine-homocysteine S-methyltransferase inhibition on hepatocyte metabolites and the proteome
skos:notation
RIV/61388963:_____/13:00394759!RIV14-GA0-61388963
n4:predkladatel
n15:ico%3A61388963
n5:aktivita
n10:P n10:I
n5:aktivity
I, P(GAP207/10/1277)
n5:cisloPeriodika
8
n5:dodaniDat
n17:2014
n5:domaciTvurceVysledku
n9:9726411 n9:9351973 n9:3046486 n9:4508394 Demianova, Zuzana
n5:druhVysledku
n11:J
n5:duvernostUdaju
n19:S
n5:entitaPredkladatele
n8:predkladatel
n5:idSjednocenehoVysledku
71953
n5:idVysledku
RIV/61388963:_____/13:00394759
n5:jazykVysledku
n14:eng
n5:klicovaSlova
apolipoprotein; fibrinogen; one-carbon metabolism; S-Adenosylmethionine; two-dimensional electrophoresis
n5:klicoveSlovo
n6:S-Adenosylmethionine n6:two-dimensional%20electrophoresis n6:fibrinogen n6:one-carbon%20metabolism n6:apolipoprotein
n5:kodStatuVydavatele
NL - Nizozemsko
n5:kontrolniKodProRIV
[BD3F3D9A3232]
n5:nazevZdroje
Biochimica Et Biophysica Acta-Proteins and Proteomics
n5:obor
n13:CE
n5:pocetDomacichTvurcuVysledku
5
n5:pocetTvurcuVysledku
6
n5:projekt
n18:GAP207%2F10%2F1277
n5:rokUplatneniVysledku
n17:2013
n5:svazekPeriodika
1834
n5:tvurceVysledku
Chrudinová, Martina Jiráček, Jiří Mládková, Jana Selicharová, Irena Demianova, Zuzana Kořínek, M.
n5:wos
000321802200017
s:issn
1570-9639
s:numberOfPages
11
n16:doi
10.1016/j.bbapap.2013.05.009