hiPSC hepatocyte model demonstrates the role of unfolded protein response and inflammatory networks in α1-antitrypsin deficiency
Cardoso De Brito, miguel
Journal of Hepatology
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Vallier, L., Segeritz, C., Rashid, S., Cardoso De Brito, m., Morell, C., Hannan, N., Gatto, L., et al. (2018). hiPSC hepatocyte model demonstrates the role of unfolded protein response and inflammatory networks in α1-antitrypsin deficiency. Journal of Hepatology, 69 (4), 851-860. https://doi.org/10.1016/j.jhep.2018.05.028
This study compared the gene expression and protein profiles of healthy liver cells and those affected by the inherited disease α1-antitrypsin deficiency. This approach identified specific factors primarily present in diseased samples which could provide new targets for drug development. This study also demonstrates the interest of using hepatic cells generated from human induced pluripotent stem cells to model liver disease in vitro for uncovering new mechanisms with clinical relevance.
StemCellInstitute, Hepatocyte, inherited liver disease, human-induced pluripotent stem cell, α1-Antitrypsin deficienc, inflammation
CPS is funded through a Children’s Liver Disease Foundation (CLDF) studentship. DAL is funded by the Medical Research Council, Wellcome Trust, GlaxoSmithKline, the Rosetrees Trust, EPSRC and UCLH NIHR Biomedical Research Centre. LV, PM, MCB, NH are funded by ERC Relieve-IMDs and ERC advanced grant New-Chol, Cambridge University Hospitals National Institute for Health Research Biomedical Research Center, and the core support grant from the Wellcome Trust and Medical Research Council to the Wellcome Trust – Medical Research Council Cambridge Stem Cell Institute. STR is funded by an MRC Clinician Scientist Fellowship award.
Alpha One Foundation (unknown)
European Commission Horizon 2020 (H2020) ERC (741707)
External DOI: https://doi.org/10.1016/j.jhep.2018.05.028
This record's URL: https://www.repository.cam.ac.uk/handle/1810/283206
Attribution 4.0 International, Attribution 4.0 International
Licence URL: http://creativecommons.org/licenses/by/4.0/
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