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Macrophage Differentiation and Polarization into an M2-Like Phenotype using a Human Monocyte-Like THP-1 Leukemia Cell Line
Published on: August 2, 2021
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Gremlin 1 is required for macrophage M2 polarization.
Liberty Mthunzi1, Simon C Rowan1, Daria S Kostyunina1
1School of Medicine, Health Sciences Centre, University College Dublin, Dublin, Ireland.
Summary
Gremlin 1 (Grem1) promotes M2-like macrophage polarization, a key process in lung fibrosis. This study reveals Grem1 is essential for this macrophage polarization, offering new insights into lung disease mechanisms.
Area of Science:
- Immunology
- Cell Biology
- Pulmonary Medicine
Background:
- Macrophage polarization to the M2-like phenotype drives fibrosis and remodeling in chronic lung diseases.
- Gremlin 1 (Grem1), a secreted glycoprotein, is expressed in lung macrophages and influences cellular functions.
- The specific role of Grem1 in M2-like macrophage polarization remained unexplored.
Purpose of the Study:
- To investigate the role of Gremlin 1 (Grem1) in the M2-like polarization of macrophages.
- To determine if Grem1 influences macrophage responses to Th2 cytokines.
Main Methods:
- Utilized recombinant Grem1 to treat mouse macrophages and bone marrow-derived macrophages (BMDMs).
- Examined M2-like polarization in response to Interleukin-4 (IL4) and Interleukin-13 (IL13).
- Employing genetic depletion of Grem1 in BMDMs and assessing the impact on M2 polarization, with partial rescue experiments using exogenous Grem1.
Main Results:
- Recombinant Grem1 enhanced M2-like polarization of mouse macrophages and BMDMs stimulated by IL4 and IL13.
- Genetic deletion of Grem1 in BMDMs significantly inhibited M2 polarization.
- Exogenous Grem1 partially restored M2 polarization in Grem1-depleted BMDMs.
Conclusions:
- Gremlin 1 (Grem1) is a required factor for M2-like polarization of macrophages.
- These findings identify a novel cellular mechanism involving Grem1 in promoting lung fibrosis and remodeling.
