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Collagen I Increases Palmitate-Induced Lipotoxicity in HepG2 Cells via Integrin-Mediated Death
TE. Maseko, E. Peterová, M. Elkalaf, D. Koutová, J. Melek, P. Staňková, V. Špalková, R. Matar, H. Lotková, Z. Červinková, O. Kučera
Jazyk angličtina Země Švýcarsko
Typ dokumentu časopisecké články
Grantová podpora
GA UK 336221
Grant Agency of the Charles University
SVV‐2023‐260656
Grant Agency of the Charles University
AZV NU21-07-00550
Ministry of Health of the Czech Republic
NETPHARM CZ.02.01.01/00/22_008/0004607
European Regional Development Fund (ERDF)
NLK
Directory of Open Access Journals
od 2011
PubMed Central
od 2011
Europe PubMed Central
od 2011
ProQuest Central
od 2011-01-01
Open Access Digital Library
od 2011-01-01
Open Access Digital Library
od 2011-01-01
Health & Medicine (ProQuest)
od 2011-01-01
ROAD: Directory of Open Access Scholarly Resources
od 2011
PubMed
39334945
DOI
10.3390/biom14091179
Knihovny.cz E-zdroje
- MeSH
- buněčná adheze * účinky léků MeSH
- buněčná smrt účinky léků MeSH
- buňky Hep G2 MeSH
- integrin alfa2beta1 metabolismus MeSH
- integriny metabolismus genetika MeSH
- kolagen typu I * metabolismus genetika MeSH
- lidé MeSH
- nealkoholová steatóza jater metabolismus patologie MeSH
- palmitany toxicita farmakologie MeSH
- proliferace buněk * účinky léků MeSH
- reaktivní formy kyslíku metabolismus MeSH
- viabilita buněk * účinky léků MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
Various strategies have been employed to improve the reliability of 2D, 3D, and co-culture in vitro models of nonalcoholic fatty liver disease, including using extracellular matrix proteins such as collagen I to promote cell adhesion. While studies have demonstrated the significant benefits of culturing cells on collagen I, its effects on the HepG2 cell line after exposure to palmitate (PA) have not been investigated. Therefore, this study aimed to assess the effects of PA-induced lipotoxicity in HepG2 cultured in the absence or presence of collagen I. HepG2 cultured in the absence or presence of collagen I was exposed to PA, followed by analyses that assessed cell proliferation, viability, adhesion, cell death, mitochondrial respiration, reactive oxygen species production, gene and protein expression, and triacylglycerol accumulation. Culturing HepG2 on collagen I was associated with increased cell proliferation, adhesion, and expression of integrin receptors, and improved cellular spreading compared to culturing them in the absence of collagen I. However, PA-induced lipotoxicity was greater in collagen I-cultured HepG2 than in those cultured in the absence of collagen I and was associated with increased α2β1 receptors. In summary, the present study demonstrated for the first time that collagen I-cultured HepG2 exhibited exacerbated cell death following exposure to PA through integrin-mediated death. The findings from this study may serve as a caution to those using 2D models or 3D scaffold-based models of HepG2 in the presence of collagen I.
Citace poskytuje Crossref.org
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