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 language | English (US) |
|---|---|
| Pages (from-to) | 1277-1286 |
| Number of pages | 10 |
| Journal | Cell Death and Differentiation |
| Volume | 11 |
| Issue number | 12 |
| DOIs | |
| State | Published - Dec 2004 |
| Externally published | Yes |
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Keywords
- Apoptosis
- Endonuclease G
- Galectin
- Human
- T lymphocyte
ASJC Scopus subject areas
- Cell Biology
Cite this
Galectin-1 induces nuclear translocation of endonuclease G in caspase- and cytochrome c-independent T cell death. / Hahn, H. P.; Pang, M.; He, J.; Hernandez, J. D.; Yang, R. Y.; Li, L. Y.; Wang, X.; Liu, Fu-Tong; Baum, L. G.
In: Cell Death and Differentiation, Vol. 11, No. 12, 12.2004, p. 1277-1286.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Galectin-1 induces nuclear translocation of endonuclease G in caspase- and cytochrome c-independent T cell death
AU - Hahn, H. P.
AU - Pang, M.
AU - He, J.
AU - Hernandez, J. D.
AU - Yang, R. Y.
AU - Li, L. Y.
AU - Wang, X.
AU - Liu, Fu-Tong
AU - Baum, L. G.
PY - 2004/12
Y1 - 2004/12
N2 - 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.
AB - 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.
KW - Apoptosis
KW - Endonuclease G
KW - Galectin
KW - Human
KW - T lymphocyte
UR - http://www.scopus.com/inward/record.url?scp=9944222484&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=9944222484&partnerID=8YFLogxK
U2 - 10.1038/sj.cdd.4401485
DO - 10.1038/sj.cdd.4401485
M3 - Article
VL - 11
SP - 1277
EP - 1286
JO - Cell Death and Differentiation
JF - Cell Death and Differentiation
SN - 1350-9047
IS - 12
ER -