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Updated: Oct 29, 2025

Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages
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Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages

Published on: June 23, 2013

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The m6A Reader IGF2BP2 Regulates Macrophage Phenotypic Activation and Inflammatory Diseases by Stabilizing TSC1 and

Xia Wang1, Yuge Ji1, Panpan Feng2

  • 1Department of Physiology School of Basic Medical Sciences Cheeloo College of Medicine Shandong University Jinan Shandong 250012 China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|July 14, 2021
PubMed

Insights

Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) regulates macrophage activation. Deleting IGF2BP2 promotes M1 macrophages, worsening colitis, but hinders M2 macrophage development, alleviating allergic inflammation.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Macrophage polarization into M1 (proinflammatory) and M2 (prohealing) phenotypes is crucial for tissue homeostasis.
  • The intrinsic molecular mechanisms governing macrophage polarization remain incompletely understood.
  • Tissue microenvironments provide cues that dictate macrophage functional states.

Purpose of the Study:

  • To investigate the role of insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) in regulating macrophage polarization.
  • To elucidate the molecular pathways through which IGF2BP2 influences M1 and M2 macrophage activation.
  • To assess the therapeutic potential of targeting IGF2BP2 in inflammatory diseases.

Main Methods:

  • Macrophage isolation and genetic deletion of IGF2BP2 (IGF2BP2-/-).
  • In vivo models of colitis (dextran sulfate sodium) and pulmonary allergic inflammation (cockroach extract).
  • Molecular analyses including mRNA and protein expression, m6A modification assays, and pathway analysis (STAT6-HMGAT1-IGF2BP2-PPARγ axis).

Main Results:

  • IGF2BP2-deleted macrophages exhibit an enhanced M1 phenotype, exacerbating dextran sulfate sodium-induced colitis.
  • IGF2BP2-deleted macrophages are refractory to IL-4 induced M2 activation and alleviate allergic inflammation.
  • IGF2BP2 facilitates the switch from M1 to M2 macrophages via targeting tuberous sclerosis 1 in an m6A-dependent manner.
  • The STAT6-HMGAT1-IGF2BP2-PPARγ axis is implicated in M2 macrophage differentiation.

Conclusions:

  • IGF2BP2 plays a critical role in regulating macrophage polarization towards an M2 phenotype.
  • IGF2BP2 acts as a molecular switch, modulating macrophage responses in inflammatory conditions.
  • Targeting IGF2BP2 presents a potential therapeutic strategy for managing inflammatory diseases by modulating macrophage activation.
Keywords:
IGF2BP2TSC1inflammatory diseasesm6A readermacrophage polarization

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