Inhibition of AMP-activated protein kinase suppresses IL-2 expression through down-regulation of NF-AT and AP-1 activation in Jurkat T cells

Bong Sook Jhun; Jung Yeon Lee; Young Taek Oh; Ju Hie Lee; Wonchae Choe; Hyung Hwan Baik; Sung Soo Kim; Kyung Sik Yoon; Joohun Ha; Insug Kang

doi:10.1016/j.bbrc.2006.10.138

Inhibition of AMP-activated protein kinase suppresses IL-2 expression through down-regulation of NF-AT and AP-1 activation in Jurkat T cells

Bong Sook Jhun
, Jung Yeon Lee
, Young Taek Oh
, Ju Hie Lee
, Wonchae Choe
, Hyung Hwan Baik
, Sung Soo Kim
, Kyung Sik Yoon
, Joohun Ha
, Insug Kang

Research output: Contribution to journal › Article › peer-review

23 Scopus citations

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)
Pages (from-to)	986-992
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	351
Issue number	4
DOIs	https://doi.org/10.1016/j.bbrc.2006.10.138
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).

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

AMPK
AP-1
CD3
GSK-3
IL-2
Ionomycin
Jurkat cells
MAPK
NF-AT
PMA

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10.1016/j.bbrc.2006.10.138

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Jhun, B. S., Lee, J. Y., Oh, Y. T., Lee, J. H., Choe, W., Baik, H. H., Kim, S. S., Yoon, K. S., Ha, J., & Kang, I. (2006). Inhibition of AMP-activated protein kinase suppresses IL-2 expression through down-regulation of NF-AT and AP-1 activation in Jurkat T cells. Biochemical and Biophysical Research Communications, 351(4), 986-992. https://doi.org/10.1016/j.bbrc.2006.10.138

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title = "Inhibition of AMP-activated protein kinase suppresses IL-2 expression through down-regulation of NF-AT and AP-1 activation in Jurkat T cells",

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.",

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author = "Jhun, \{Bong Sook\} and Lee, \{Jung Yeon\} and Oh, \{Young Taek\} and Lee, \{Ju Hie\} and Wonchae Choe and Baik, \{Hyung Hwan\} and Kim, \{Sung Soo\} and Yoon, \{Kyung Sik\} and Joohun Ha and Insug Kang",

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).",

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AU - Jhun, Bong Sook

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AU - Lee, Ju Hie

AU - Choe, Wonchae

AU - Baik, Hyung Hwan

AU - Kim, Sung Soo

AU - Yoon, Kyung Sik

AU - Ha, Joohun

AU - Kang, Insug

N1 - 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).

PY - 2006/12/29

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N2 - 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.

AB - 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.

KW - AMPK

KW - AP-1

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KW - IL-2

KW - Ionomycin

KW - Jurkat cells

KW - MAPK

KW - NF-AT

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ER -

Inhibition of AMP-activated protein kinase suppresses IL-2 expression through down-regulation of NF-AT and AP-1 activation in Jurkat T cells

Abstract

Bibliographical note

UN SDGs

Keywords

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