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Title 

α-Melanocyte-stimulating hormone inhibits lipopolysaccharide-induced tumor necrosis factor-α production in leukocytes by modulating protein kinase A, p38 kinase, and nuclear factor κB signaling pathway

Authors 

Sun Woo YoonSung-Ho GohJ S ChunEun Wie ChoMyung Kyu LeeK L KimJ J KimC J KimHaryoung Poo

Publisher 

American Society for Biochemistry and Molecular Biology

Issue Date 

2003

Citation 

Journal of Biological Chemistry, vol. 278, no. 35, pp. 32914-32920

Keywords 

biochemistrychemical activationpolysaccharidestumorssurface receptorshormonesalpha intermedincyclic AMP dependent protein kinaseimmunoglobulin enhancer binding proteinlipopolysaccharide

Abstract 

The neuropeptide α-melanocyte-stimulating hormone (α-MSH) inhibits inflammation by down-regulating the expression of proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) in leukocytes via stimulation of α-MSH cell surface receptors. However, the signaling mechanism of α-MSH action has not yet been clearly elucidated. Here, we have investigated signaling pathways by which α-MSH inhibits lipopolysaccharide (LPS)-induced TNF-α production in leukocytes such as THP-1 cells. We focused on the possible roles of protein kinase A (PKA), p38 kinase, and nuclear factor κB (NFκB) signaling. In THP-1 cells, LPS is known to activate p38 kinase, which in turn activates NFκB to induce TNF-α production. We found that pretreatment of cells with α-MSH blocked LPS-induced p38 kinase and NFκB activation as well as TNF-α production. This response was proportional to α-MSH receptor expression levels, and addition of an α-MSH receptor antagonist abolished the inhibitory effects. In addition, α-MSH treatment activated PKA, and PKA inhibition abrogated the inhibitory effects of α-MSH on p38 kinase activation, NFκB activation, and TNF-α production. Taken together, our results indicate that stimulation of PKA by α-MSH causes inhibition of LPS induced activation of p38 kinase and NFκB to block TNF-α production.

ISSN 

0021-9258

Link 

http://dx.doi.org/10.1074/jbc.M302444200

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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