Structural/functional relationships between internal and external MSH receptors: Modulation of expression in Cloudman melanoma cells by UVB radiation
Version of Record online: 15 FEB 2005
Copyright © 1991 Wiley-Liss, Inc.
Journal of Cellular Physiology
Volume 147, Issue 1, pages 1–6, April 1991
How to Cite
Chakraborty, A. K., Orlow, S. J., Bolognia, J. L. and Pawelek, J. M. (1991), Structural/functional relationships between internal and external MSH receptors: Modulation of expression in Cloudman melanoma cells by UVB radiation. J. Cell. Physiol., 147: 1–6. doi: 10.1002/jcp.1041470102
- Issue online: 15 FEB 2005
- Version of Record online: 15 FEB 2005
- Manuscript Accepted: 17 DEC 1990
- Manuscript Received: 24 SEP 1990
Expression of internal receptors for MSH is an important criterion for responsiveness to MSH by Cloudman melanoma cells (Orlow et al: J. Cell. Physiol., 142: 129–136, 1990). Here, we show that internal and external receptors for MSH are of identical molecular weights (50–53 kDa) and share common antigenic determinants, indicating a structural relationship between the 2 populations of molecules. The internal receptors co-purified with a sub-cellular fraction highly enriched for small vesicles, many of which were coated. Ultraviolet B light (UVB) acted synergistically with MSH to increase tyrosinase activity and melanin content of cultured Cloudman melanoma cells, consistent with previous findings in the skin of mice and guinea pigs (Bologniaet al: J. Invest. Derm., 92:651–656, 1989). Preceding the rise in tyrosinase activity in cultured cells, UVB elicited a decrease in internal MSH binding sites and a concomittant increase in external sites. The time frame for the UVB effects on MSH receptors and melanogenesis, 48 hours, was similar to that for a response to solar radiation in humans. Together, the results indicate a key role for MSH receptors in the induction of melanogenesis by UVB and suggest a potential mechanism of action for UVB: redistribution of MSH receptors with a resultant increase in cellular responsiveness to MSH.