NDLI: Adiponectin inhibits pro-inflammatory signaling in human macrophages independent of interleukin-10.

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Adiponectin inhibits pro-inflammatory signaling in human macrophages independent of interleukin-10.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Libby, Peter López-ilasaca, Marco Folco, Eduardo J. Rocha, Viviane Z.
Description	Author Affiliation: Folco EJ ( Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.)
Abstract	Macrophages participate pivotally in the pathogenesis of many chronic inflammatory diseases including atherosclerosis. Adiponectin, a vasculoprotective molecule with insulin-sensitizing and anti-atherogenic properties, suppresses pro-inflammatory gene expression in macrophages by mechanisms that remain incompletely understood. This study investigated the effects of adiponectin on major pro-inflammatory signaling pathways in human macrophages. We demonstrate that pretreatment of these cells with adiponectin inhibits phosphorylation of nuclear factor kappaB inhibitor (IkappaB), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK), induced by either lipopolysaccharide (LPS) or tumor necrosis factor (TNF) alpha, as well as STAT3 phosphorylation induced by interleukin-6 (IL6). Antagonism of IL10 by either neutralizing antibodies or siRNA-mediated silencing did not abrogate the anti-inflammatory actions of adiponectin, indicating that the ability of adiponectin to render human macrophages tolerant to various pro-inflammatory stimuli does not require this cytokine. A systematic search for adiponectin-inducible genes with established anti-inflammatory properties revealed that adiponectin augmented the expression of A20, suppressor of cytokine signaling (SOCS) 3, B-cell CLL/lymphoma (BCL) 3, TNF receptor-associated factor (TRAF) 1, and TNFAIP3-interacting protein (TNIP) 3. These results suggest that adiponectin triggers a multifaceted response in human macrophages by inducing the expression of various anti-inflammatory proteins that act at different levels in concert to suppress macrophage activation.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	38
Volume Number	284
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2009-09-18
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Interleukin-10 Pharmacology MAP Kinase Signaling System Drug Effects Macrophages Metabolism Adiponectin Cell Line DNA-Binding Proteins Gene Expression Regulation I-kappa B Proteins Inflammation Interleukin-6 Intracellular Signaling Peptides And Proteins JNK Mitogen-Activated Protein Kinases Lipopolysaccharides Nuclear Proteins Biosynthesis Phosphorylation Proteins Proto-Oncogene Proteins STAT3 Transcription Factor TNF Receptor-Associated Factor 1 Transcription Factors Tumor Necrosis Factor-alpha P38 Mitogen-Activated Protein Kinases Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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