MSH receptor expression and the relationship to melanogenesis and metastatic activity in B16 melanoma

Lunec, John; Pieron, Cora; Aj, Thody

doi:10.1097/00008390-199205000-00002

Cited by 39 publications

(23 citation statements)

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“…Thus, the abili ty of the ligands to bind to the receptor does not appear to relate to their biological potency. A similar discrepancy between receptor binding and biological activity has been observed in murine melanoma cells [15].…”

Section: Introductionsupporting

confidence: 72%

“…However, Hunt et al [24,27] POMC gene expression has been demonstrated in mu rine and hamster melanoma cells [67] and an immunoreactive a-MSH-like peptide has been identified in human and murine melanoma cells [68], This raises the possibili ty that, in melanoma cells at least, POMC peptides may have an autocrine function in stimulating proliferation. POMC peptides have also been shown to affect experi mental metastasis of murine melanoma cells [15]. 18 Hunt Response of Human Melanocytes to MSH While melanin per se may not provide adequate protec tion against UV-induced damage, the actual synthesis of melanin may have a role in protecting against free radical damage.…”

Section: The Effect Of Msh On Melanocyte Morphologymentioning

confidence: 99%

“…In the studies of Hunt et al [24,26,27], approximately a third of cultures were unresponsive, and those cultures which failed to respond to MSH were also unresponsive to 15 ACTH. In an earlier study, Iwata et al [35] demonstrated that NDP-MSH failed to stimulate tyrosinase activity in 50% of human foreskin organ cultures and responsiveness was unrelated to the racial origin of the skin.…”

Section: Introductionmentioning

confidence: 99%

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Melanocyte-Stimulating Hormone: A Regulator of Human Melanocyte Physiology

Hunt

1995

Pathobiology

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Although the melanocyte-stimulating hormone (MSH) is well-recognised as a pigmentary hormone in animals, its role in human pigmentation is still a matter for conjecture, not least because cultured human melanocytes have proved to be relatively refractory to the peptide. However, recent work has shown that human melanocytes can respond to MSH peptides and the related adrenocorticotropic hormone. While the pigmentary responses are the most studied, they are by no means the only effects of these peptides on human melanocytes. This article reviews recent work on the responses of human melanocytes to MSH peptides and demonstrates that these peptides may be key regulators of human melanocyte physiology.

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Section: Introductionsupporting

confidence: 72%

Section: The Effect Of Msh On Melanocyte Morphologymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Melanocyte-Stimulating Hormone: A Regulator of Human Melanocyte Physiology

Hunt

1995

Pathobiology

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“…The POMC immunoreactivity has also been reported in cross sections of human skin (81). Melanoma cells and normal human melanocytes express receptors at least for MSH and presumptively also for ACTH, as both of these peptides have been shown to stimulate melanogenesis in cultured human melanocytes (82)(83)(84)(85). Circulating MSH and ACTH from extracutaneous sources are assumed to be responsible for the hyperpigmentation observed in patients with Addison's disease, pituitary tumors and carcinomas with ectopic production of these peptides.…”

Section: Proopiomelanocortin (Pomc) and Its Derived Peptidesmentioning

confidence: 99%

Mechanisms of Ultraviolet Light‐Induced Pigmentation

Gilchrest

Park

Eller

et al. 1996

Photochem & Photobiology

323

231

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“…These cells predominantly express the MC1R receptor. 19,20 All forms of NDPMSH were equipotent in their ability to antagonize 125 I-NDPMSH binding to the cells (not shown). We then examined whether iodination affected the agonist effect on MC1R with respect to cAMP accumulation.…”

Section: Rationale For Using Ndpmshmentioning

confidence: 92%

Effects of a potent melanocortin agonist on the diabetic/obese phenotype in yellow mice

et al. 1998

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OBJECTIVE: To test the hypothesis that a melanocortin agonist can reverse obesity and insulin resistance in mice overexpressing the agouti protein. EXPERIMENTAL MODEL: Mice overexpressing the agouti protein either by transgene introduction (b b-actin promotor) or by mutation (A y ). DESIGN: NDPMSH was tested for pharmacokinetic suitability. NDPMSH at various doses was administered subcutaneously twice a day for 2 ± 3 weeks. MEASUREMENTS: Fur pigmentation, various fatness parameters (core temperature, fat pad weight and body weight), blood glucose and hormones, fatty acid synthase measurement. RESULTS: NDPMSH caused fur pigmentation and core temperature changes, but failed to affect any metabolic parameters in agouti-dependent manner. CONCLUSION: NDPMSH, as a representation melanocortin agonist, does not compete with agouti in reversing agoutidependent metabolic effects. This suggests that 1) agouti works via a receptor other than a melanocortin receptor to mediate its metabolic effects, 2) agouti-dependent metabolic effects are mediated through melanocortin receptors but not via antagonism of these receptors, or 3) NDPMSH is pharmacodynamically an inappropriate molecule for these types of studies.

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MSH receptor expression and the relationship to melanogenesis and metastatic activity in B16 melanoma

Cited by 39 publications

References 0 publications

Melanocyte-Stimulating Hormone: A Regulator of Human Melanocyte Physiology

Melanocyte-Stimulating Hormone: A Regulator of Human Melanocyte Physiology

Mechanisms of Ultraviolet Light‐Induced Pigmentation

Effects of a potent melanocortin agonist on the diabetic/obese phenotype in yellow mice

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