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Updated: Jul 12, 2026

Bone Marrow-derived Macrophage Production
Published on: November 22, 2013
Expression of macrophage asialoglycoprotein-binding protein is induced through MAPK classical pathway
R Katsuyama1, A Morioka, S Oka
1Department of Biological Chemistry and CREST (Core Research for Educational Science and Technology) Project, Japan Science and Technology Corporation, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, 606-8501, Japan.
Abstract:
Macrophage asialoglycoprotein-binding protein (M-ASGP-BP) is a Gal/GalNAc-specific lectin, which functions as an endocytosis receptor. We found that the expression of M-ASGP-BP mRNA in bone marrow cells was induced during the differentiation into macrophages. To investigate the mechanism by which M-ASGP-BP mRNA expression is induced, we used U937 cells as a model. Treatment of U937 cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) resulted in M-ASGP-BP mRNA expression within 6 h. This induction was completely inhibited by PKC inhibitors, calphostin C, and staurosporine. Furthermore, MAP kinase inhibitors PD98059, but not SB202190, blocked M-ASGP-BP mRNA expression. These data indicate that M-ASGP-BP mRNA expression occurs through the activation of PKC and the MAPK classical pathway in the course of cell differentiation into macrophages.
Insights
Macrophage asialoglycoprotein-binding protein (M-ASGP-BP) mRNA expression is induced during macrophage differentiation. Protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) pathways mediate this M-ASGP-BP induction.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Macrophage asialoglycoprotein-binding protein (M-ASGP-BP) is a Gal/GalNAc-specific lectin.
- M-ASGP-BP functions as an endocytosis receptor.
- M-ASGP-BP mRNA expression is induced during macrophage differentiation from bone marrow cells.
Purpose of the Study:
- To investigate the molecular mechanisms underlying M-ASGP-BP mRNA induction during macrophage differentiation.
- To utilize U937 cells as a model system for studying M-ASGP-BP gene regulation.
Main Methods:
- U937 cells were treated with 12-O-tetradecanoylphorbol-13-acetate (TPA) to induce differentiation.
- The effects of protein kinase C (PKC) inhibitors (calphostin C, staurosporine) and mitogen-activated protein kinase (MAPK) inhibitors (PD98059, SB202190) on M-ASGP-BP mRNA expression were assessed.
Main Results:
- TPA treatment rapidly induced M-ASGP-BP mRNA expression in U937 cells within 6 hours.
- PKC inhibitors completely blocked TPA-induced M-ASGP-BP mRNA expression.
- The MAPK inhibitor PD98059, but not SB202190, inhibited M-ASGP-BP mRNA expression, suggesting involvement of the classical MAPK pathway.
Conclusions:
- M-ASGP-BP mRNA expression during macrophage differentiation is mediated by the activation of PKC.
- The classical MAPK pathway is also involved in the induction of M-ASGP-BP mRNA.
- These findings elucidate key signaling pathways regulating M-ASGP-BP expression in differentiating macrophages.
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