Abstract
AMP-activated protein kinase (AMPK) is a key regulator of energy homeostasis and its activation during T cell receptor stimulation has recently been reported. In this study, we examined the role of AMPK in interleukin (IL)-2 production in T cells. Inhibition of AMPK by compound C, a specific inhibitor of AMPK or small interfering RNA of AMPKα1 suppressed IL-2 production in Jurkat T cells and peripheral blood lymphocytes stimulated with PMA plus ionomycin (PMA/Io) or with monoclonal anti-CD3 plus anti-CD28. We then showed that AMPK inhibition reduced PMA/Io-induced IL-2 mRNA expression and IL-2 promoter activation. Moreover, inhibition of AMPK suppressed transcriptional activation of NF-AT and AP-1, but not NF-κB, in PMA/Io-activated Jurkat cells. Finally, we found that compound C inhibited PMA/Io-induced phosphorylation of p38, JNK, and GSK-3β but not of ERK. These results suggest that AMPK mediates IL-2 production by regulating NF-AT and AP-1activation during T cell stimulation.
Original language | English (US) |
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Pages (from-to) | 986-992 |
Number of pages | 7 |
Journal | Biochemical and Biophysical Research Communications |
Volume | 351 |
Issue number | 4 |
DOIs | |
State | Published - Dec 29 2006 |
Externally published | Yes |
Bibliographical note
Funding Information:This work was supported by the Korea Research Foundation Grant funded by the Korean Government (MOEHRD) (KRF-2004-015-E00071; KRF-2004-531-E00015) and by Grants from the Korea Science and Engineering Foundation (R13-2002-020-01001-001-0; R01-2006-000-10517-0).
Keywords
- AMPK
- AP-1
- CD3
- GSK-3
- IL-2
- Ionomycin
- Jurkat cells
- MAPK
- NF-AT
- PMA