A+T rich interaction domain protein 3a (Arid3a) impairs Mertk-mediated efferocytosis in cholestasis
Abstract
Background & aims Macrophages are key elements in the pathogenesis of cholestatic liver diseases. Arid3a plays a prominent role in the biologic properties of hematopoietic stem cells, B lymphocytes and tumor cells, but its ability to modulate macrophage function during cholestasis remains unknown. Methods Gene and protein expression and cellular localization were assessed by q-PCR, immunohistochemistry, immunofluorescence staining and flow cytometry. We generated myeloid-specific Arid3a knockout mice and established three cholestatic murine models. The transcriptome was analyzed by RNA-seq. A specific inhibitor of the Mertk receptor was used in vitro and in vivo. Promoter activity was determined by chromatin immunoprecipitation-seq against Arid3a and a luciferase reporter assay. Results In cholestatic murine models, myeloid-specific deletion of Arid3a alleviated cholestatic liver injury (accompanied by decreased accumulation of macrophages). Arid3a-deficient macrophages manifested a more reparative phenotype, which was eliminated by in vitro treatment with UNC2025, a specific inhibitor of the efferocytosis receptor Mertk. Efferocytosis of apoptotic cholangiocytes was enhanced in Arid3a-deficient macrophages via upregulation of Mertk. Arid3a negatively regulated Mertk transcription by directly binding to its promoter. Targeting Mertk in vivo effectively reversed the protective phenotype of Arid3a deficiency in macrophages. Arid3a was upregulated in hepatic macrophages and circulating monocytes in primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC). Mertk was correspondingly upregulated and negatively correlated with Arid3a expression in PBC and PSC. Mertk+ cells were located in close proximity to cholangiocytes, while Arid3a+ cells were scattered among immune cells with greater spatial distances to hyperplastic cholangiocytes in PBC and PSC. Conclusions Arid3a promotes cholestatic liver injury by impairing Mertk-mediated efferocytosis of apoptotic cholangiocytes by macrophages during cholestasis. The Arid3a-Mertk axis is a promising novel therapeutic target for cholestatic liver diseases. Impact and implications Macrophages play an important role in the pathogenesis of cholestatic liver diseases. This study reveals that macrophages with Arid3a upregulation manifest a pro-inflammatory phenotype and promote cholestatic liver injury by impairing Mertk-mediated efferocytosis of apoptotic cholangiocytes during cholestasis. Although we now offer a new paradigm to explain how efferocytosis is regulated in a myeloid cell autonomous manner, the regulatory effects of Arid3a on chronic liver diseases remain to be further elucidated.
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Arid3a, a newly identified primary biliary cholangitis risk gene, affects the efferocytosis of apoptotic biliary epithelial cells mediated by macrophages, which promotes cholestasis in both primary biliary cholangitis and primary sclerosing cholangitis.
“Arid3a, a newly identified primary biliary cholangitis risk gene, affects the efferocytosis of apoptotic BECs mediated by macrophages, which promotes cholestasis in both primary biliary cholangitis and primary sclerosing cholangitis.45”
From Primary biliary cholangitis. (2024) · cites this paper as [45]
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“…to the damaged liver via treatment with the dual CCR2/CCR5 antagonist (Guicciardi et al., 2018), via myeloid-specific deletion of Arid3a (Chen et al., 2023), or via IFNγ depletion (Ravichandran et al., 2019) diminishes periportal fibrosis, thus suggesting that Mφ accumulation in…”
InfluentialLi, H., Chen, D., Zhang, X., Chen, R., Fang, S., Zhao, F., Nie, W., Zhou, Z., 徐万纹, Zhao, Z., et al. (2026) · Genes & Diseases · doi:10.1016/j.gendis.2026.102410
Self-citationJiang, X., Ma, J., Liu, Z., & Chen, J. (2026) · Frontiers in Pharmacology · doi:10.3389/fphar.2026.1955615
“MerTK is a member of the TAM receptor tyrosine kinase family and an important efferocytic receptor expressed by hepatic macrophages (Triantafyllou et al., 2018; Chen et al., 2023).”
- Authors
- Chen, R., Huang, B., Lian, M., Wei, Y., Miao, Q., Liang, J., Ou, Y., Liang, X., Zhang, H., Li, Y., Xiao, X., Wang, Q., You, Z., Chai, J., Gershwin, M. E., Tang, R., & Ma, X.
- Affiliations
- Shanghai Jiao Tong University (CN)
- Fudan University (CN)
- Army Medical University (CN)
- University of California, Davis (US)
- Corresponding author
- Gershwin, M. Eric
- Tang, Ruqi
- Ma, Xiong
- ORCID
- Venue
- Journal of Hepatology
- Publisher
- Elsevier BV
- Published
- 2023-12
- Volume
- 79
- Issue
- 6
- Pages
- 1478-1490
- ISSN
- 0168-8278 (ISSN-L)
- OpenAlex
- W4386376733
- Cited by
- 39
- References
- 47
- Citations by year
- 2026: 12 · 2025: 16 · 2024: 8 · 2023: 3
- FWCI
- 6.59
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Hepatology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Innovative Research Team of High-level Local Universities in Shanghai
- National Natural Science Foundation of China (81570469, 81620108002, 81790634, 81830016, 81873561, 81922010, 82000532, 82070581, 82130017, 82270663)
- Shanghai Municipal Education Commission
- Shanghai Municipality Science and Technology Commission
- Shanghai Rising-Star Program (22QA1405500)
- Topics
- Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- ARID3A, MERTK, efferocytosis, cholestasis, macrophages, cholestatic liver injury, primary biliary cirrhosis, primary sclerosing cholangitis, transcriptional regulation, myeloid-specific knockout, hepatic macrophages
- MeSH terms
- c-Mer Tyrosine Kinase, Animals, Cholestasis, DNA-Binding Proteins, Liver Diseases, Macrophages, Phagocytosis, Transcription Factors, Mice, Knockout, Mice
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