Involvement of IGF-1 and Akt in M1/M2 activation state in bone marrow-derived macrophages
Abstract
Macrophages can be polarised to adopt the M1 or M2 phenotype and functional outcomes of activation include altered secretion of immune molecules such as insulin-like growth factor (IGF)-1 as well as upregulation of cell surface molecules specifically associated with each state. Interleukin (IL)-4 mediates its effects through two receptors, the type I and II receptors and activation of these receptors results in phosphorylation of signal transducers and activators of transcription (STAT)6. JAK3 is activated as a consequence of ligation of the type I IL-4R, which participates in Akt activation. We set out to investigate the impact of perturbation of IGF-1 tone on IL-4- and interferon (IFN)γ-induced activation, the mechanisms by which this may occur and the contribution of type I IL-4R activation to adoption of the M2 state. The data presented here indicate that IL-4-induced activation of Akt is JAK3-dependent, enhanced by release of IGF-1 and necessary for full adoption of the M2 phenotype, since blocking IGF-1 activity blunts the ability of IL-4 to induce activation of Akt and to upregulate expression of some M2-associated molecules. In addition, differential control of the expression of mannose receptor (MRC1), arginase-1 (Arg-1), chitinase-3 like 3 (Chi3l3) and found in inflammatory zone 1 (FIZZ1) was observed. The IFNγ-induced decrease in IGF-1 was exacerbated by inhibition of phosphatidylinositol-3 (PI3) kinase, indicating that Akt may regulate its own activation via IGF-1. Overall, a deficit in IGF-1/Akt signalling is associated with decreased capacity to induce the M2 state and an increased responsiveness to IFNγ.
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Igf1 expression is inhibited by pro-inflammatory stimuli and enhanced in anti-inflammatory environments.
“Our findings, in line with previous studies (59,68–71), show that Igf1 expression is inhibited by pro-inflammatory stimuli and enhanced in anti-inflammatory environments.”
From <i>Trem2</i> promotes anti-inflammatory responses in microglia and is suppressed under pro-inflammatory conditions (2020) · cites this paper as [71]
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- Authors
- Barrett, J. P., Minogue, A. M., Falvey, A., & Lynch, M. A.
- Affiliations
- Trinity College Dublin (IE)
- Corresponding author
- Minogue, Aedín M.
- Venue
- Experimental Cell Research
- Publisher
- Elsevier BV
- Published
- 2015-07
- Volume
- 335
- Issue
- 2
- Pages
- 258-268
- ISSN
- 0014-4827 (ISSN-L)
- OpenAlex
- W773459996
- Cited by
- 59
- References
- 29
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 7 · 2023: 7 · 2022: 7 · 2021: 7 · 2020: 6 · 2019: 5 · 2018: 5 · 2017: 7 · 2016: 2 · 2015: 2
- FWCI
- 2.62
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Experimental Cell Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Science Foundation Ireland (07/IN.1/B949)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › Mast cells and histamine
- Keywords
- insulin-like growth factor I, Akt signaling, macrophage polarization, M2 macrophages, M1 macrophages, bone marrow-derived macrophages, IL-4, JAK3, interferon-gamma, PI3K signaling, arginase-1, Fizz1, STAT6
- MeSH terms
- Animals, Cells, Cultured, Insulin-Like Growth Factor I, Macrophage Activation, Macrophages, Signal Transduction, Interleukin-4, Proto-Oncogene Proteins c-akt, Mice, Janus Kinase 3, Transcriptome
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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