The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Eosinophils secrete IL-4 to facilitate liver regeneration
Open accessAbstract
The liver is a central organ for the synthesis and storage of nutrients, production of serum proteins and hormones, and breakdown of toxins and metabolites. Because the liver is susceptible to toxin- or pathogen-mediated injury, it maintains a remarkable capacity to regenerate by compensatory growth. Specifically, in response to injury, quiescent hepatocytes enter the cell cycle and undergo DNA replication to promote liver regrowth. Despite the elucidation of a number of regenerative factors, the mechanisms by which liver injury triggers hepatocyte proliferation are incompletely understood. We demonstrate here that eosinophils stimulate liver regeneration after partial hepatectomy and toxin-mediated injury. Liver injury results in rapid recruitment of eosinophils, which secrete IL-4 to promote the proliferation of quiescent hepatocytes. Surprisingly, signaling via the IL-4Rα in macrophages, which have been implicated in tissue repair, is dispensable for hepatocyte proliferation and liver regrowth after injury. Instead, IL-4 exerts its proliferative actions via IL-4Rα in hepatocytes. Our findings thus provide a unique mechanism by which eosinophil-derived IL-4 stimulates hepatocyte proliferation in regenerating liver.
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Cites
Alternative activation of macrophages
Gordon, S. (2003) · Nature Reviews Immunology · doi:10.1038/nri978 · Cited by 6,189
Protective and pathogenic functions of macrophage subsets
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Macrophage-specific PPARγ controls alternative activation and improves insulin resistance
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“As described previously (33), quantitative real-time PCR analyses were carried out with cDNA templates using SsoFast EvaGreen Supermix (Biorad).”
MethodSelf-citationLiver regeneration: from myth to mechanism
Taub, R. (2004) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1489 · Cited by 1,567
Alternatively activated macrophages produce catecholamines to sustain adaptive thermogenesis
Nguyen, K. D., Qiu, Y., Cui, X., Goh, Y. P. S., Mwangi, J., David, T., Mukundan, L., Brombacher, F., Locksley, R. M., & Chawla, A. (2011) · Nature · doi:10.1038/nature10653 · Cited by 1,038
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“To address this issue, we performed 70% hepatectomy in congenic wild-type (WT) and ΔdblGATA mice, with the latter lacking eosinophils because of a mutation in the promoter region of the Gata1 gene (16).”
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Cited by
Macrophages in Tissue Repair, Regeneration, and Fibrosis
Wynn, T. A., & Vannella, K. M. (2016) · Immunity · doi:10.1016/j.immuni.2016.02.015 · Cited by 4,481
Inflammation and metabolism in tissue repair and regeneration
Eming, S. A., Wynn, T. A., & Martin, P. (2017) · Science · doi:10.1126/science.aam7928 · Cited by 1,369
Type 2 immunity in tissue repair and fibrosis
Gieseck, R. L., Wilson, M. S., & Wynn, T. A. (2018) · Nature Reviews Immunology · doi:10.1038/nri.2017.90 · Cited by 1,055
Rao, R. R., Long, J. Z., White, J. P., Svensson, K. J., Lou, J., Lokurkar, I., Jedrychowski, M. P., Ruas, J. L., Wrann, C. D., Lo, J. C., et al. (2014) · Cell · doi:10.1016/j.cell.2014.03.065 · Cited by 973
Macrophages, Immunity, and Metabolic Disease
McNelis, J. C., & Olefsky, J. M. (2014) · Immunity · doi:10.1016/j.immuni.2014.05.010 · Cited by 720
Metadata
- Authors
- Goh, Y. P. S., Henderson, N. C., Heredia, J. E., Red Eagle, A., Odegaard, J. I., Lehwald, N., Nguyen, K. D., Sheppard, D., Mukundan, L., Locksley, R. M., & Chawla, A.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2013-05-28
- Volume
- 110
- Issue
- 24
- Pages
- 9914-9919
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2065833808
- Cited by
- 277
- References
- 8
- FWCI
- 10.46
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Goh, Y. P. S., Henderson, N. C., Heredia, J. E., Red Eagle, A., Odegaard, J. I., Lehwald, N., Nguyen, K. D., Sheppard, D., Mukundan, L., Locksley, R. M., & Chawla, A. (2013). Eosinophils secrete IL-4 to facilitate liver regeneration. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1304046110
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