Regulation of TNF-alpha secretion by a specific melanocortin-1 receptor peptide agonist

Peptides. 2003 May;24(5):709-16. doi: 10.1016/s0196-9781(03)00127-x.

Abstract

The lack of specific pharmacological tools has impeded the evaluation of the role of each melanocortin receptor (MCR) subtype in the myriad physiological effects of melanocortins. 154N-5 is an octapeptide (MFRdWFKPV-NH(2)) that was first identified as an MC1R antagonist in Xenopus melanophores [J. Biol. Chem. 269 (1994) 29846]. In this manuscript, we show that 154N-5 is a specific agonist for human and murine MC1R. The peptide has negligible activity at MC3R and MC4R and is 25-fold less potent and a weak agonist at MC5R. 154N-5 was tested in both a cellular and an animal model of tumor necrosis factor-alpha (TNF-alpha) secretion. The inhibitory efficacy of 154N-5 on TNF-alpha secretion in both models was similar to the nonselective agonist NDP-alpha-melanocyte stimulating hormone (NDP-alphaMSH), thus, we conclude that inhibition of TNF-alpha secretion by melanocortin peptides is mediated by MC1R. 154N-5 is a valuable new tool for the evaluation of specific contribution of MC1R agonism to physiological and pathological processes.

MeSH terms

  • Animals
  • Cell Line
  • Dose-Response Relationship, Drug
  • Female
  • Humans
  • Ligands
  • Lipopolysaccharides / pharmacology
  • Mice
  • Peptide Fragments / agonists
  • Peptide Fragments / chemistry
  • Peptide Fragments / pharmacology*
  • RNA, Messenger / metabolism
  • Receptor, Melanocortin, Type 1 / agonists*
  • Receptor, Melanocortin, Type 1 / analysis
  • Receptors, Melanocortin / agonists
  • Tumor Necrosis Factor-alpha / biosynthesis*

Substances

  • 154N-5 peptide
  • Ligands
  • Lipopolysaccharides
  • Peptide Fragments
  • RNA, Messenger
  • Receptor, Melanocortin, Type 1
  • Receptors, Melanocortin
  • Tumor Necrosis Factor-alpha