Endogenous galectin-3 is localized in membrane lipid rafts and regulates migration of dendritic cells

Daniel K. Hsu, Alexander I. Chernyavsky, Huan Yuan Chen, Lan Yu, Sergei A. Grando, Fu-Tong Liu

Research output: Contribution to journalArticle

72 Scopus citations

Abstract

This study reveals a function of endogenous galectin-3, an animal lectin recognizing β-galactosides, in regulating dendritic cell motility both in vitro and in vivo, which to our knowledge is unreported. First, galectin-3-deficient (gal3-/-) bone marrow-derived dendritic cells exhibited defective chemotaxis compared to gal3+/+ cells. Second, cutaneous dendritic cells in gal3-/- mice displayed reduced migration to draining lymph nodes upon hapten stimulation compared to gal3+/+ mice. Moreover, gal3-/- mice were impaired in the development of contact hypersensitivity relative to gal3+/+ mice in response to a hapten, a process in which dendritic cell trafficking to lymph nodes is critical. In addition, defective signaling was detected in gal3-/- cells upon chemokine receptor activation. By immunofluorescence microscopy, we observed that galectin-3 is localized in membrane ruffles and lamellipodia in stimulated dendritic cells and macrophages. Furthermore, galectin-3 was enriched in lipid raft domains under these conditions. Finally, we determined that ruffles on gal3-/- cells contained structures with lower complexity compared to gal3+/+ cells. In view of the participation of membrane ruffles in signal transduction and cell motility, we conclude that galectin-3 regulates cell migration by functioning at these structures.

Original languageEnglish (US)
Pages (from-to)573-583
Number of pages11
JournalJournal of Investigative Dermatology
Volume129
Issue number3
DOIs
StatePublished - Mar 2009

ASJC Scopus subject areas

  • Dermatology
  • Biochemistry
  • Cell Biology
  • Molecular Biology

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