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Galectin-4 Interaction with CD14 Triggers the Differentiation of Monocytes into Macrophage-like Cells via the MAPK Signaling Pathway.
Hong, So-Hee; Shin, Jun-Seop; Chung, Hyunwoo; Park, Chung-Gyu.
Affiliation
  • Hong SH; Xenotransplantation Research Center, Seoul National University College of Medicine, Seoul 03080, Korea.
  • Shin JS; Institute of Endemic Diseases, Seoul National University College of Medicine, Seoul 03080, Korea.
  • Chung H; Cancer Research Institute, Seoul National University College of Medicine, Seoul 03080, Korea.
  • Park CG; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea.
Immune Netw ; 19(3): e17, 2019 Jun.
Article in En | MEDLINE | ID: mdl-31281714
ABSTRACT
Galectin-4 (Gal-4) is a ß-galactoside-binding protein mostly expressed in the gastrointestinal tract of animals. Although intensive functional studies have been done for other galectin isoforms, the immunoregulatory function of Gal-4 still remains ambiguous. Here, we demonstrated that Gal-4 could bind to CD14 on monocytes and induce their differentiation into macrophage-like cells through the MAPK signaling pathway. Gal-4 induced the phenotypic changes on monocytes by altering the expression of various surface molecules, and induced functional changes such as increased cytokine production and matrix metalloproteinase expression and reduced phagocytic capacity. Concomitant with these changes, Gal-4-treated monocytes became adherent and showed elongated morphology with higher expression of macrophage markers. Notably, we found that Gal-4 interacted with CD14 and activated the MAPK signaling cascade. Therefore, these findings suggest that Gal-4 may exert the immunoregulatory functions through the activation and differentiation of monocytes.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: Immune Netw Year: 2019 Document type: Article

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: Immune Netw Year: 2019 Document type: Article