期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 65, 期 -, 页码 270-279出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2013.06.038
关键词
Peroxiredoxin V; LPS; IL-6; Jak2/Stat5 pathway
资金
- National Research Foundation of Korea (NRF)
- Korea government (MEST) [20120009425]
- Korean Health Technology R&D Project, Ministry of Health & Welfare, Republic of Korea [A111455]
- Republic of Korea
- Korea Health Promotion Institute [A111455] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Mammalian peroxiredoxin V (PrdxV) is a niultifunctional protein that protects cells from DNA damage and inhibits stress-induced apoptosis. However, PrdxV is also known to be involved in modulating lipopolysaccharide (LPS)-induced host cell signaling, but its precise role is not fully understood. In this study, we used stably transfected RAW264.7 cells and transiently transfected 293-mTLR4-MD2-CD14 cells expressing wild-type (WT) or mutant (C48S) PrdxV to characterize the function and mechanism of action of PrdxV in LPS-induced immune responses. We found that PrdxV selectively reduces production of interleukin 6 (IL-6) by inhibiting activation of signal transducer and activator of transcription 5 (Stat5) through interaction with Jak2. Notably, this activity of PrdxV was dependent on its catalytic Cys48 residue, but not its peroxidase activity. The binding of to Jak2 effectively inhibited Jak2 phosphorylation, but PrdxV did not act as efficiently as SOCS1 (suppressor of cytokine signaling I). Our results suggest that PrdxV is a key mediator contributing to the regulation of LPS/TLR4-induced immune responses. (C) 2013 The Authors. Published by Elsevier Inc. All rights reserved.
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