Galectin-1 induces nuclear translocation of endonuclease G in caspase- and cytochrome c-independent T cell death

H. P. Hahn, M. Pang, J. He, J. D. Hernandez, R. Y. Yang, L. Y. Li, X. Wang, Fu-Tong Liu, L. G. Baum

Research output: Contribution to journalArticle

115 Scopus citations

Abstract

Galectin-1, a mammalian lectin expressed in many tissues, induces death of diverse cell types, including lymphocytes and tumor cells. The galectin-1 T cell death pathway is novel and distinct from other death pathways, including those initiated by Fas and corticosterolds. We have found that galectin-1 binding to human T cell lines triggered rapid translocation of endonuclease G from mitochondria to nuclei. However, endonuclease G nuclear translocation occurred without cytochrome c release from mitochondria, without nuclear translocation of apoptosis-inducing factor, and prior to loss of mitochondrial membrane potential. Galectin-1 treatment did not result in caspase activation, nor was death blocked by caspase inhibitors. However, galectin-1 cell death was inhibited by intracellular expression of galectin-3, and galectin-3 expression inhibited the eventual loss of mitochondrial membrane potential. Galectin-1-induced cell death proceeds via a caspase-independent pathway that involves a unique pattern of mitochondrial events, and different galectin family members can coordinately regulate susceptibility to cell death.

Original languageEnglish (US)
Pages (from-to)1277-1286
Number of pages10
JournalCell Death and Differentiation
Volume11
Issue number12
DOIs
StatePublished - Dec 2004
Externally publishedYes

Keywords

  • Apoptosis
  • Endonuclease G
  • Galectin
  • Human
  • T lymphocyte

ASJC Scopus subject areas

  • Cell Biology

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    Hahn, H. P., Pang, M., He, J., Hernandez, J. D., Yang, R. Y., Li, L. Y., Wang, X., Liu, F-T., & Baum, L. G. (2004). Galectin-1 induces nuclear translocation of endonuclease G in caspase- and cytochrome c-independent T cell death. Cell Death and Differentiation, 11(12), 1277-1286. https://doi.org/10.1038/sj.cdd.4401485