Loss of FOXA2 induces ER stress and hepatic steatosis and alters developmental gene expression in human iPSC-derived hepatocytes
Open accessAbstract
FOXA2 has been known to play important roles in liver functions in rodents. However, its role in human hepatocytes is not fully understood. Recently, we generated FOXA2 mutant induced pluripotent stem cell (FOXA2−/−iPSC) lines and illustrated that loss of FOXA2 results in developmental defects in pancreatic islet cells. Here, we used FOXA2−/−iPSC lines to understand the role of FOXA2 on the development and function of human hepatocytes. Lack of FOXA2 resulted in significant alterations in the expression of key developmental and functional genes in hepatic progenitors (HP) and mature hepatocytes (MH) as well as an increase in the expression of ER stress markers. Functional assays demonstrated an increase in lipid accumulation, bile acid synthesis and glycerol production, while a decrease in glucose uptake, glycogen storage, and Albumin secretion. RNA-sequencing analysis further validated the findings by showing a significant increase in genes associated with lipid metabolism, bile acid secretion, and suggested the activation of hepatic stellate cells and hepatic fibrosis in MH lacking FOXA2. Overexpression of FOXA2 reversed the defective phenotypes and improved hepatocyte functionality in iPSC-derived hepatic cells lacking FOXA2. These results highlight a potential role of FOXA2 in regulating human hepatic development and function and provide a human hepatocyte model, which can be used to identify novel therapeutic targets for FOXA2-associated liver disorders.
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Expression of HNF1A, HNF4A, and FOXA2 typically peaks during the early progenitor stage and decreases toward the final hepatocyte-like cell stage.
“This finding is consistent with other reports that these genes’ expression typically peaks during early progenitor stage and decreases towards the final hepatocyte-like cells stage24–26.”
From Temporal proteomic profiling of iPSC-derived human liver organoids reveals optimal maturation for drug metabolism and toxicology (2026) · cites this paper as [26]
The Results section on FOXA2 expression during differentiation reports a peak at days 6–8 followed by a decline to little or no expression at the mature hepatocyte stage. The paper does not establish the same early peak and subsequent decline for HNF1A or HNF4A; its measurements of those genes concern FOXA2-deficient cells rather than their expression over the differentiation timeline. Page numbers are not available in our copy. (LLM, conf=0.88)
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- Authors
- Aghadi, M., Elgendy, R., & Abdelalim, E. M.
- Affiliations
- Hamad bin Khalifa University (QA)
- AstraZeneca (Sweden) (SE)
- Corresponding author
- Abdelalim, Essam M.
- Venue
- Cell Death & Disease
- Published
- 2022-08-16
- Volume
- 13
- Issue
- 8
- Pages
- 713-713
- ISSN
- 2041-4889 (ISSN-L)
- PMC
- PMC9381545
- OpenAlex
- W4292004267
- Cited by
- 36
- References
- 53
- Citations by year
- 2026: 5 · 2025: 10 · 2024: 9 · 2023: 11 · 2022: 1
- FWCI
- 4.61
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Cell Death and Disease (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- Qatar National Research Fund (NPRP10-1221-160041)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pluripotent Stem Cells Research
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Keywords
- FOXA2, endoplasmic reticulum stress, hepatic steatosis, iPSC-derived hepatocytes, hepatic progenitor cells, lipid accumulation, bile acid synthesis, hepatic stellate cells, liver fibrosis, liver development, glucose uptake, glycogen storage, albumin secretion
- MeSH terms
- Bile Acids and Salts, Cell Differentiation, Fatty Liver, Humans, Liver, Hepatocytes, Genes, Developmental, Hepatocyte Nuclear Factor 3-beta, Induced Pluripotent Stem Cells, Endoplasmic Reticulum Stress
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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