Abstract
Background
Repeated exposures to ultraviolet B radiation (UVB) induce pigmented spots on dorsal
skin of (HR-1 × HR/De) F1 hairless mouse. We showed previously that this mouse is suitable for studies of melanocyte
function.
Objective
To clarify the mechanism of development of pigmented spots induced by chronic UVB
exposure.
Methods
We used light and fluorescence microscopy to quantify changes in the numbers of differentiated
melanocytes containing melanin pigments (MM) and melanoblasts/melanocytes immunohistochemically
positive for tyrosinase-related protein (TRP)-1, TRP-2 (dopachrome tautomerase), and
c-kit in epidermis during the development of pigmented spots in hairless mice chronically
exposed to UVB (99 mJ/cm2, 3 times/week, 8 weeks).
Results
The change in the number of TRP-1-positive cells during chronic UVB exposure was similar
to that of MM: both increased dramatically during the stage of acute pigmentation,
then decreased sharply after cessation of UVB, concomitantly with depigmentation;
subsequently they increased gradually with the development of pigmented spots. In
contrast, after two UVB exposures, no c-kit-positive cells were detected, then the
number gradually increased during UVB irradiation, and continued to increase after
cessation of irradiation; TRP-2-positive cells showed a rather similar pattern, except
that they did not disappear initially.
Conclusion
Our results indicate that chronic UVB irradiation induces differentiation and proliferation
of melanoblasts, followed by an increase of differentiated melanocytes, leading to
the development of pigmented spots. The sequence of expression of markers appeared
to be c-kit, TRP-2, TRP-1, and finally melanin, as it is during normal melanocyte
differentiation.
Keywords
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Article info
Publication history
Published online: July 12, 2010
Accepted:
March 25,
2009
Received in revised form:
February 21,
2009
Received:
November 10,
2008
Identification
Copyright
© 2009 Japanese Society for Investigative Dermatology. Published by Elsevier Inc. All rights reserved.