IL-4 augments anisomycin-induced p38 activation via Akt pathway in a follicular dendritic cell (FDC)-like line

Hyang Mi Lee; Hyung Sung Jin; Jae Won Park; Sun Mi Park; Hye Kyung Jeon; Tae H. Lee

doi:10.1016/S0014-5793(03)00800-7

IL-4 augments anisomycin-induced p38 activation via Akt pathway in a follicular dendritic cell (FDC)-like line

Hyang Mi Lee, Hyung Sung Jin, Jae Won Park, Sun Mi Park, Hye Kyung Jeon, Tae H. Lee

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13 Citations (Scopus)

Abstract

Follicular dendritic cells (FDCs) play pivotal roles in germinal center (GC) responses in secondary lymphoid follicles, and their functions are influenced by cytokines present in the GC. We investigated the functional effects of interleukin-4 (IL-4) using an established FDC-like line of HK cells. In spite of the activation of ERK1/2 and PI3K/Akt pathways by IL-4, which are implicated in the induction of cell proliferation and survival, IL-4 did not exhibit protective function on anisomycin-induced apoptosis of HK cells, but rather slightly enhanced it. This IL-4 effect correlated with the up-regulation of anisomycin-induced p38 signaling, which is attenuated by inhibition of the PI3K/Akt pathway. Expression of an active form of Akt increased anisomycin-elicited activation of p38 and its upstream kinase MKK3/6. Our data indicate a positive cross-talk between the p38 and PI3K/Akt pathways.

Original language	English
Pages (from-to)	110-114
Number of pages	5
Journal	FEBS Letters
Volume	549
Issue number	1-3
DOIs	https://doi.org/10.1016/S0014-5793(03)00800-7
Publication status	Published - 2003 Aug 14

Bibliographical note

Funding Information:
We thank Dr. Walsh for providing adenoviruses expressing β-galactosidase and myr-Akt. This work was supported by the grant from the Ministry of Health and Welfare (02-PJ1-PG3-21203-0009) and by grants from Protein Network Research Center (Yonsei University) and Immunoregulatory Center (University of Ulsan), the Ministry of Science and Technology/Korea Science and Engineering Foundation, Korea.

All Science Journal Classification (ASJC) codes

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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title = "IL-4 augments anisomycin-induced p38 activation via Akt pathway in a follicular dendritic cell (FDC)-like line",

abstract = "Follicular dendritic cells (FDCs) play pivotal roles in germinal center (GC) responses in secondary lymphoid follicles, and their functions are influenced by cytokines present in the GC. We investigated the functional effects of interleukin-4 (IL-4) using an established FDC-like line of HK cells. In spite of the activation of ERK1/2 and PI3K/Akt pathways by IL-4, which are implicated in the induction of cell proliferation and survival, IL-4 did not exhibit protective function on anisomycin-induced apoptosis of HK cells, but rather slightly enhanced it. This IL-4 effect correlated with the up-regulation of anisomycin-induced p38 signaling, which is attenuated by inhibition of the PI3K/Akt pathway. Expression of an active form of Akt increased anisomycin-elicited activation of p38 and its upstream kinase MKK3/6. Our data indicate a positive cross-talk between the p38 and PI3K/Akt pathways.",

author = "Lee, {Hyang Mi} and Jin, {Hyung Sung} and Park, {Jae Won} and Park, {Sun Mi} and Jeon, {Hye Kyung} and Lee, {Tae H.}",

note = "Funding Information: We thank Dr. Walsh for providing adenoviruses expressing β-galactosidase and myr-Akt. This work was supported by the grant from the Ministry of Health and Welfare (02-PJ1-PG3-21203-0009) and by grants from Protein Network Research Center (Yonsei University) and Immunoregulatory Center (University of Ulsan), the Ministry of Science and Technology/Korea Science and Engineering Foundation, Korea.",

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AU - Park, Sun Mi

AU - Jeon, Hye Kyung

AU - Lee, Tae H.

N1 - Funding Information: We thank Dr. Walsh for providing adenoviruses expressing β-galactosidase and myr-Akt. This work was supported by the grant from the Ministry of Health and Welfare (02-PJ1-PG3-21203-0009) and by grants from Protein Network Research Center (Yonsei University) and Immunoregulatory Center (University of Ulsan), the Ministry of Science and Technology/Korea Science and Engineering Foundation, Korea.

PY - 2003/8/14

Y1 - 2003/8/14

N2 - Follicular dendritic cells (FDCs) play pivotal roles in germinal center (GC) responses in secondary lymphoid follicles, and their functions are influenced by cytokines present in the GC. We investigated the functional effects of interleukin-4 (IL-4) using an established FDC-like line of HK cells. In spite of the activation of ERK1/2 and PI3K/Akt pathways by IL-4, which are implicated in the induction of cell proliferation and survival, IL-4 did not exhibit protective function on anisomycin-induced apoptosis of HK cells, but rather slightly enhanced it. This IL-4 effect correlated with the up-regulation of anisomycin-induced p38 signaling, which is attenuated by inhibition of the PI3K/Akt pathway. Expression of an active form of Akt increased anisomycin-elicited activation of p38 and its upstream kinase MKK3/6. Our data indicate a positive cross-talk between the p38 and PI3K/Akt pathways.

AB - Follicular dendritic cells (FDCs) play pivotal roles in germinal center (GC) responses in secondary lymphoid follicles, and their functions are influenced by cytokines present in the GC. We investigated the functional effects of interleukin-4 (IL-4) using an established FDC-like line of HK cells. In spite of the activation of ERK1/2 and PI3K/Akt pathways by IL-4, which are implicated in the induction of cell proliferation and survival, IL-4 did not exhibit protective function on anisomycin-induced apoptosis of HK cells, but rather slightly enhanced it. This IL-4 effect correlated with the up-regulation of anisomycin-induced p38 signaling, which is attenuated by inhibition of the PI3K/Akt pathway. Expression of an active form of Akt increased anisomycin-elicited activation of p38 and its upstream kinase MKK3/6. Our data indicate a positive cross-talk between the p38 and PI3K/Akt pathways.

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IL-4 augments anisomycin-induced p38 activation via Akt pathway in a follicular dendritic cell (FDC)-like line

Abstract

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