Abstract:
:The neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) is a powerful suppressor of inflammation mediated by macrophages, which express at least two receptors, melanocortin 1 and 3 receptors (MC1r and MC3r) that bind alpha-MSH. Albeit, the anti-inflammatory activity of alpha-MSH has been well documented in macrophages, the mechanisms of alpha-MSH activity in macrophages are not clearly understood. This study is to investigate which of the MCr expressed on macrophages is associated with the immunosuppressive activities of alpha-MSH on LPS-stimulated macrophages. To address this question, we transfected RAW264.7 macrophage cells with MC1r small interfering (si)RNA, which specifically targets mouse MC1r mRNA. The diminution of MC1r mRNA expression was 82% at 24 h and 67% at 48 h after transfection. There was a significant loss in alpha-MSH suppression of NO generation and TNF-alpha production by MC1r siRNA-transfected macrophages stimulated with LPS. There was an equally diminished alpha-MSH suppression of LPS-stimulated intracellular activation of NF-kappaB and p38 phosphorylation. In addition, the diminishment of MC1r expression by siRNA transfection had no influence on MC3r expression and function in the macrophages. These findings demonstrate that alpha-MSH suppression of LPS-induced inflammatory activity in macrophages requires expression of MC1r. The results imply that although all of the MCr are G-coupled proteins, they may not necessarily function through the same intracellular pathways in macrophages.
journal_name
J Leukoc Bioljournal_title
Journal of leukocyte biologyauthors
Li D,Taylor AWdoi
10.1189/jlb.0707463subject
Has Abstractpub_date
2008-07-01 00:00:00pages
191-8issue
1eissn
0741-5400issn
1938-3673pii
jlb.0707463journal_volume
84pub_type
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