Although the pathogenesis of alopecia areata (AA) has been associated with lipid peroxidation,
the role of antioxidants has not been fully explored [
1
,
2
]. Heme oxygenase-1 (HO-1) is the rate-limiting enzyme in the catabolism of heme; it
breaks down the porphyrin ring to yield equal molar amounts of free iron, carbon monoxide
and biliverdin, which is subsequently reduced to bilirubin. Among three different
isoforms of HO, the inducible isoform of HO-1, also known as the major 32 kDa heat shock protein HSP-32, is induced by a wide variety of stressful stimuli,
including ultraviolet irradiation, hydrogen peroxide, lipopolysaccharides, and organic
chemicals [
3
,
4
]. HO-1 also inhibits T cell-dependent skin inflammation and differentiation as well
as the function of antigen-presenting cells [
[5]
]. The upregulation of HO-1 expression in inflamed skin such as psoriasis and cutaneous
wounds has suggested that HO-1 might play an important cytoprotective role under conditions
of cellular stress such as ischemia, hypoxia, inflammation, and oxidative stress [
6
,
7
]. However, the role of HO-1 in AA has not been studied. To elucidate the pathogenetic
role of HO-1 in AA, we compared the HO-1 expression between AA patches and normal
skin.Keywords
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References
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- Antioxidant enzymes and lipid peroxidation in the scalp of patients with alopecia areata.J Dermatol Sci. 2002; 29: 85-90
Article info
Publication history
Published online: July 12, 2010
Received:
August 5,
2008
Identification
Copyright
© 2009 Japanese Society for Investigative Dermatology. Published by Elsevier Inc. All rights reserved.
