α-MSH causes a small rise in cAMP but has no effect on basal or ultraviolet-stimulated melanogenesis in human melanocytes

Friedmann, Peter S.; Wren, Fiona E.; Buffey, J.; MacNeil, Sheila

doi:10.1111/j.1365-2133.1990.tb01841.x

Cited by 59 publications

(26 citation statements)

References 10 publications

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“…Only a few studies focused on endothelial-tubular epithelial cell interactions (9,12). They mainly used a sandwich coculture method culturing endothelial cells on confluent monolayers of tubular epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

Migration of leukocytes across an endothelium-epithelium bilayer as a model of renal interstitial inflammation

Bijuklic

Jennings

Kountchev³

et al. 2007

American Journal of Physiology-Cell Physiology

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Migration of leukocytes across an endothelium-epithelium bilayer as a model of renal interstitial inflammation. Am J Physiol Cell Physiol 293: C486-C492, 2007. First published April 11, 2007 doi:10.1152/ajpcell.00419.2006.-Interstitial inflammation has emerged as a key event in the development of acute renal failure. To gain better insight into the nature of these inflammatory processes, the interplay between tubular epithelial cells, endothelial cells, and neutrophils (PMN) was investigated. A coculture transmigration model was developed, composed of human dermal microvascular endothelial (HDMEC) and human renal proximal tubular cells (HK-2) cultured on opposite sides of Transwell growth supports. Correct formation of an endoepithelial bilayer was verified by light and electron microscopy. The model was used to study the effects of endotoxin (LPS), tumor necrosis factor (TNF)-␣, and ␣-melanocyte-stimulating hormone (␣-MSH) by measuring PMN migration and cytokine release. To distinguish between individual roles of microvascular endothelial and epithelial cells in transmigration processes, migration of PMN was investigated separately in HK-2 and HDMEC monolayers. Sequential migration of PMN through endothelium and epithelium could be observed and was significantly increased after proinflammatory stimulation with either TNF-␣ or LPS (3.5 Ϯ 0.58 and 2.76 Ϯ 0.64-fold vs. control, respectively). Coincubation with ␣-MSH inhibited the transmigration of PMN through the bilayer after proinflammatory stimulation with LPS but not after TNF-␣. The bilayers produced significant amounts of IL-8 and IL-6 mostly released from the epithelial cells. Furthermore, ␣-MSH decreased LPS-induced IL-6 secretion by 30% but had no significant effect on IL-8 secretion. We established a transmigration model showing sequential migration of PMN across microvascular endothelial and renal tubular epithelial cells stimulated by TNF-␣ and LPS. Anti-inflammatory effects of ␣-MSH in this bilayer model are demonstrated by inhibition on PMN transmigration and IL-6 secretion.coculture; polymorphonuclear neutrophil migration; HK-2; interleukin-8; interleukin-6; ␣-melanocyte-stimulating hormone

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Section: Discussionmentioning

confidence: 99%

Migration of leukocytes across an endothelium-epithelium bilayer as a model of renal interstitial inflammation

Bijuklic

Jennings

Kountchev³

et al. 2007

American Journal of Physiology-Cell Physiology

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“…More recently, the group of Dr. B. Gilchrest (27) has shown that tyrosinase is phosphorylated through a PKC-dependent pathway and that over-expression of PKC-b in non-pigmented melanoma cells leads to the phosphorylation and activation of tyrosinase (27). However, this hypothesis has not been unanimously approved, since several reports have clearly shown that melanogenesis is not affected or even stimulated by the inhibition of PKC (26,28).…”

Section: Direct Effects Of Uv On Melanocytesmentioning

confidence: 99%

Cyclic AMP a Key Messenger in the Regulation of Skin Pigmentation

Buscà

Ballotti

2000

Pigment Cell Research

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640

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In humans, stimulation of skin pigmentation over the basal constitutive level, which we commonly call tanning, is physiologically stimulated by ultraviolet (UV) radiation of the solar light. UV-induced skin darkening involves an increase in the melanocyte number as well as a stimulation of melanin neosynthesis and melanocyte dendricity, a crucial morphological feature required for melanin transfer to keratinocytes. These events, corresponding to the final steps of melanocyte differentiation, play a central role in the tanning response and are subjected to an accurate research which aims to understand the precise mechanisms governing their regulation. In the present review, we will mainly focus our attention on the molecular processes involved in the regulation of melanogenesis.

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“…a-MSH is a very potent stimulator of the pigmentation and differentiation of pigmented cells, including melanoma cells (Schwahn et al, 2001). POMC derived peptides have been shown to transmit their signal via G-protein coupled receptors through the formation of cyclic AMP and activation of protein kinase C (Friedmann et al, 1990;Ao et al, 1998;AbdelMalek et al, 2000). Five different subtypes of melanocortin receptors with different tissue distribution have been described (Chhajlani and Wikberg, 1992;Mountjoy et al, 1992;Chhajlani et al, 1993;Gantz et al, 1993a,b).…”

mentioning

confidence: 99%

Tissue distribution and differential expression of melanocortin 1 receptor, a malignant melanoma marker

Salazar‐Onfray

López

Lundqvist³

et al. 2002

Br J Cancer

106

111

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The melanocortin 1 receptor is a G-protein-coupled receptor, described to be expressed on melanomas and melanocytes. Subsequent RT -PCR studies demonstrated the presence of melanocortin 1 receptor mRNA in other tissues such as pituitary gland and testis. Previously, we have demonstrated that three HLA-A2 binding nonamer peptides derived from melanocortin 1 receptor can elicit peptide-specific CTL which can recognize target cells transfected with the melanocortin 1 receptor gene and MHC class I matched melanoma lines. The potential of targeting melanocortin 1 receptor in therapy and diagnosis will depend on a preferential expression of this receptor in the majority of primary and metastatic melanomas vs normal tissues. We tested a panel of melanomas, carcinomas and other cell lines for the presence of melanocortin 1 receptor, using two monoclonal antibodies. The receptor was detected in 83% of the tested melanoma cell lines but not in other carcinoma lines. Immunohistochemistry revealed a strong expression of melanocortin 1 receptor in all tested primary and metastatic melanomas, but also demonstrated low levels of expression in adrenal medulla, cerebellum, liver and keratinocytes. Flow cytometry studies showed that melanocortin 1 receptor was expressed in in vitro activated monocytes/macrophages and in the THP-1 monocytic leukaemia line at levels of about 1 in 3 to 1 in 5 of that found in melanomas. Peripheral blood-derived dendritic cells, also express melanocortin 1 receptor in vitro. This extensive analysis of melanocortin 1 receptor tissue distribution may be of relevance not only for melanoma immunology, but also for research on the pathogenicity of inflammatory conditions in the skin and neurologic tissues. It remains to be seen if the over-expression of melanocortin 1 receptor in melanomas is sufficiently high to allow a 'therapeutic window' to be exploited in cancer immunotherapy.

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α-MSH causes a small rise in cAMP but has no effect on basal or ultraviolet-stimulated melanogenesis in human melanocytes

Cited by 59 publications

References 10 publications

Migration of leukocytes across an endothelium-epithelium bilayer as a model of renal interstitial inflammation

Migration of leukocytes across an endothelium-epithelium bilayer as a model of renal interstitial inflammation

Cyclic AMP a Key Messenger in the Regulation of Skin Pigmentation

Tissue distribution and differential expression of melanocortin 1 receptor, a malignant melanoma marker

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