Abstract
Background
Cyclooxygenase-2 (COX2) plays an important role in the production of prostaglandin
E2 (PGE2), which is made by epidermal keratinocytes in response to ultraviolet radiation
(UVR). PGE2 is important for the proliferation and melanogenesis of epidermal melanocytes,
the loss of which leads to vitiligo. COX2-1195A > G, -765G > C, and -8473T > C polymorphisms may influence the mRNA levels of COX2 and affect the production of
PGE2 subsequently. Therefore, we supposed that these polymorphisms may be associated
with vitiligo.
Objective
The aim of the study was to elucidate the association between three functional COX2 polymorphisms and the risk of vitiligo.
Methods
This was a hospital-based, case–control study of 755 vitiligo patients and 774 vitiligo-free
controls who were frequency matched by age and sex. We genotyped COX2-1195A>G, -765G>C, and -8473T>C polymorphisms by using PCR-restriction fragment length polymorphism (RFLP) method
and assessed their respective associations with the risk of vitiligo in Han Chinese
populations.
Results
We found a statistically significant increased risk of vitiligo to be associated with
the COX2-1195 G variant allele (p = 0.004). Significantly higher vitiligo risks were found among subgroups with these
characteristics: age >20 years, male, active, nonsegmental vitiligo, and onset age >20 years. In addition,
the interaction between COX2-1195 and COX2-8473 was statistically significant (p = 0.004).
Conclusion
For the first time, we provide evidence that functional polymorphisms in the COX2 gene may influence the risk of vitiligo in Han Chinese populations, suggesting new
clues that help to clarify the pathogenesis of vitiligo. Larger studies are needed
to verify these findings.
Keywords
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Article info
Publication history
Published online: July 12, 2010
Accepted:
September 25,
2008
Received in revised form:
September 20,
2008
Received:
July 28,
2008
Identification
Copyright
© 2008 Japanese Society for Investigative Dermatology. Published by Elsevier Inc. All rights reserved.