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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
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Galectin-3 shapes microglial phenotype through endogenous and exogenous mechanisms
Lluís Camprubí-Ferrer1, Yiyi Yang1, Rosalía Fernández-Calle1
1Experimental Neuroinflammation Laboratory, Department of Experimental Medical Sciences, Lund University, Lund, Sweden.
Frontiers in Cellular Neuroscience
|January 5, 2026
Summary
Galectin-3 (Gal3) regulates microglial cell functions, including energy, movement, and inflammatory responses. This study defines Gal3
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Galectin-3 (Gal3) is a lectin secreted by microglia, impacting brain homeostasis and disease.
- Understanding Gal3's intracellular and extracellular roles is crucial for neuroinflammation research.
Purpose of the Study:
- To investigate the distinct roles of endogenous and exogenous Galectin-3 (Gal3) in microglial physiology.
- To elucidate Gal3's influence on microglial energetic control, receptor expression, and inflammatory signaling.
Main Methods:
- Generated Gal3-deficient BV2 microglial cells.
- Assessed microglial physiology using genetic deletion and recombinant Gal3.
- Utilized internalization assays and analyzed receptor expression (CD11b, TREM2, Clec7a, CD45).
- Examined Syk phosphorylation, NOX2 expression, and TNFα release.
- Studied Gal3's role in the 5xFAD Alzheimer's disease mouse model.
Main Results:
- Gal3 deletion increased microglial cell area, mitochondrial activity, and motility.
- Endogenous Gal3 maintains CD11b surface levels and restrains TREM2/Clec7a expression.
- Exogenous Gal3 promoted CD45 internalization and paracrine TNFα release.
- Synergistic requirement of endogenous/exogenous Gal3 for Syk phosphorylation and NOX2 expression.
- Endogenous Gal3 constrained phagocytosis; exogenous Gal3 enhanced endocytosis.
- In 5xFAD mice, Gal3 absence elevated Clec7a levels around plaques without altering microgliosis.
Conclusions:
- Galectin-3 is a critical regulator of microglial homeostasis, uptake, receptor expression, and inflammatory signaling.
- A novel regulatory mechanism involving endogenous and exogenous Gal3 pools in microglia is defined.
- A new Gal3-Clec7a interaction is identified, highlighting Gal3's role in modulating microglial phenotype and neuroinflammation.
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