The neuropeptide α-MSH has specific receptors on neutrophils and reduces chemotaxis in vitro

Catania, Anna; Rajora, Nilum; Capsoni, F.; Minonzio, Francesca; Star, Robert A.; Lipton, James M.

doi:10.1016/0196-9781(96)00037-x

Cited by 191 publications

(147 citation statements)

References 23 publications

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“…In mammals, there have been several studies investigating a possible role of MC1R in the immune system. MC1R is expressed in many leucocytes (Catania et al 1996;Neumann et al 2001) and the melanocortin peptide a-MSH, which is an MC1R agonist, has well-established anti-inflammatory effects (Star et al 1995). However, no evidence of immune dysfunction has been reported in mice or humans which lack functional MC1R.…”

Section: Why Mc1r?mentioning

confidence: 99%

A window on the genetics of evolution:MC1Rand plumage colouration in birds

2005

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Melanins are a ubiquitous component of plumage colouration in birds and serve a wide variety of functions. Although the genetic control of melanism has been studied in chickens and other domestic species, little was known about the molecular genetics of melanin distribution in wild birds until recently. Studies have now revealed that a single locus, the melanocortin-1 receptor (MC1R) locus, is responsible for melanic polymorphisms in at least three unrelated species: the bananaquit, the snow goose and the arctic skua. Results show that melanism was a derived trait and allow other evolutionary inferences about the history of melanism to be made. The role of MC1R in plumage patterning is surprisingly diverse among different species. The conserved molecular basis for the evolution of melanism in birds and several other vertebrates is probably related to low pleiotropic effects at the MC1R.

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Section: Why Mc1r?mentioning

confidence: 99%

A window on the genetics of evolution:MC1Rand plumage colouration in birds

2005

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“…[10][11][12][13][14][15] These effects are mediated by cell surface, G-protein-coupled, melanocortin receptors (MC-R). [16][17][18][19] aMSH binding to MC-R1 and MC-R5 activates adenyl cyclase and results in a significant increase of intracellular cAMP. 20,21 In melanocytes this event up-regulates expression of tyrosinase, an enzyme that converts tyrosine to melanin.…”

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confidence: 99%

Generation of expression constructs that secrete bioactive αMSH and their use in the treatment of experimental autoimmune encephalomyelitis

et al. 2003

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a Melanocyte-stimulating hormone (aMSH) is a 13 amino acid peptide with potent anti-inflammatory effects. We created two DNA expression constructs (miniPOMC and pACTH1-17) that encode bioactive versions of the aMSH peptide, and tested these constructs for therapeutic effects in experimental autoimmune encephalomyelitis (EAE). Each construct contained the sequences for aMSH, as well as the sequences that are involved in the secretion and processing of the POMC gene with the assumption that these sequences would promote processing and release of the encoded aMSH peptide. The differences between the two constructs lie at the C-terminal end where amino acids necessary for amidation of aMSH were included in only the pACTH1-17 construct. These two constructs were tested in vitro in bioassays, and in vivo in a mouse model of EAE. The results show that although bioactive peptides are secreted from cells transfected with either construct, there appears to be a significant therapeutic effect only with the pACTH1-17 construct which contains the extra C-terminal amino acids. The data suggest that it is possible to engineer DNA expression vectors encoding small secreted peptides such as aMSH, and that similar type constructs may be useful as therapeutics for the treatment of inflammatory diseases.

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“…To test the idea that the primary ␣-MSH receptor MC-1, recently found in murine macrophages and in human macrophages and neutrophils (Star et al, 1995;Rajora et al, 1996;Catania et al, 1996), likewise occurs in brain tissue, normal mouse brain was subjected to RT-PCR and Southern analysis. This analysis revealed a substantial signal at 529 bp, consistent with the size of the cDNA for the murine MC-1 receptor (Fig.…”

Section: Evidence Of Mc-1 Receptor Expression In the Brainmentioning

confidence: 99%

α-MSH Modulates Local and Circulating Tumor Necrosis Factor-α in Experimental Brain Inflammation

et al. 1997

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Tumor necrosis factor (TNF-α) underlies pathological processes and functional disturbances in acute and chronic neurological disease and injury. The neuroimmunomodulatory peptide α-MSH modulates actions and production of proinflammatory cytokines including TNF-α, but there is no prior evidence that it alters TNF-α induced within the brain. To test for this potential influence of the peptide, TNF-α was induced centrally by local injection of bacterial lipopolysaccharide (LPS). α-MSH given once i.c.v. with LPS challenge, twice daily intraperitoneally (i.p.) for 5 d between central LPS injections, or both i.p. and centrally, inhibited production of TNF-α within brain tissue. Inhibition of TNF-α protein formation by α-MSH was confirmed by inhibition of TNF-α mRNA. Plasma TNF-α concentration was elevated markedly after central LPS, indicative of an augmented peripheral host response induced by the CNS signal. The increase was inhibited by α-MSH treatments, in relation to inhibition of central TNF-α. Presence within normal mouse brain of mRNA for the α-MSH receptor MC-1 suggests that the inhibitory effects of α-MSH on brain and plasma TNF-α might be mediated by this receptor subtype. The inhibitory effect of α-MSH on brain TNF-α did not depend on circulating factors because the effect also occurred in brain tissuein vitro. This indicates that α-MSH can act directly on brain cells to inhibit their production of TNF-α. If central TNF-α contributes to pathology in CNS disease and injury, and promotes inflammation in the periphery, agents that act on brain α-MSH receptors should decrease the pathological TNF-α reaction and promote tissue survival.

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The neuropeptide α-MSH has specific receptors on neutrophils and reduces chemotaxis in vitro

Cited by 191 publications

References 23 publications

A window on the genetics of evolution:MC1Rand plumage colouration in birds

A window on the genetics of evolution:MC1Rand plumage colouration in birds

Generation of expression constructs that secrete bioactive αMSH and their use in the treatment of experimental autoimmune encephalomyelitis

α-MSH Modulates Local and Circulating Tumor Necrosis Factor-α in Experimental Brain Inflammation

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