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Sökning: WFRF:(Ewart L) > Modelling human liv...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004043naa a2200637 4500
001oai:gup.ub.gu.se/309245
003SwePub
008240528s2021 | |||||||||||000 ||eng|
0247 a https://gup.ub.gu.se/publication/3092452 URI
0247 a https://doi.org/10.1038/s42003-021-02616-x2 DOI
040 a (SwePub)gu
041 a eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Kostrzewski, T.4 aut
2451 0a Modelling human liver fibrosis in the context of non-alcoholic steatohepatitis using a microphysiological system
264 c 2021-09-15
264 1b Springer Science and Business Media LLC,c 2021
520 a Kostrzewski et al. introduce an in vitro microphysiological model of non-alcoholic steatohepatitis (NASH), consisting of co-cultured primary human liver cells. The authors characterised the transcriptomic, inflammatory and fibrotic phenotype of the model and show that major features of NASH can be recapitulated and therapeutic interventions mimicked. Non-alcoholic steatohepatitis (NASH) is a common form of chronic liver disease characterised by lipid accumulation, infiltration of immune cells, hepatocellular ballooning, collagen deposition and liver fibrosis. There is a high unmet need to develop treatments for NASH. We have investigated how liver fibrosis and features of advanced clinical disease can be modelled using an in vitro microphysiological system (MPS). The NASH MPS model comprises a co-culture of primary human liver cells, which were cultured in a variety of conditions including+/- excess sugar, fat, exogenous TGF beta or LPS. The transcriptomic, inflammatory and fibrotic phenotype of the model was characterised and compared using a system biology approach to identify conditions that mimic more advanced clinical disease. The transcriptomic profile of the model was shown to closely correlate with the profile of patient samples and the model displayed a quantifiable fibrotic phenotype. The effects of Obeticholic acid and Elafibranor, were evaluated in the model, as wells as the effects of dietary intervention, with all able to significantly reduce inflammatory and fibrosis markers. Overall, we demonstrate how the MPS NASH model can be used to model different aspects of clinical NASH but importantly demonstrate its ability to model advanced disease with a quantifiable fibrosis phenotype.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicin0 (SwePub)3022 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicine0 (SwePub)3022 hsv//eng
653 a term-follow-up
653 a obeticholic acid
653 a preclinical models
653 a disease
653 a pathogenesis
653 a multicenter
653 a progression
653 a cirrhosis
653 a patterns
653 a agonist
653 a Life Sciences & Biomedicine - Other Topics
653 a Science & Technology - Other
653 a Topics
7001 a Snow, S.4 aut
7001 a Battle, A. L.4 aut
7001 a Peel, S.4 aut
7001 a Ahmad, Z.4 aut
7001 a Basak, J.4 aut
7001 a Surakala, M.4 aut
7001 a Bornot, A.4 aut
7001 a Lindgren, J.4 aut
7001 a Ryaboshapkina, M.4 aut
7001 a Clausen, M.4 aut
7001 a Lindén, Daniel,d 1971u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology4 aut
7001 a Maass, C.4 aut
7001 a Young, L. M.4 aut
7001 a Corrigan, A.4 aut
7001 a Ewart, L.4 aut
7001 a Hughes, D.4 aut
7102 a Göteborgs universitetb Institutionen för neurovetenskap och fysiologi4 org
7730 t Communications Biologyd : Springer Science and Business Media LLCg 4:1q 4:1x 2399-3642
8564 u https://www.nature.com/articles/s42003-021-02616-x.pdf
8564 8u https://gup.ub.gu.se/publication/309245
8564 8u https://doi.org/10.1038/s42003-021-02616-x

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