Abstract
Abnormal histone modification by histone deacetylases (HDACs), including HDAC1 and sirtuin 1 (SIRT1), has been reported to play an important role in the pathogenesis of psoriasis by altering cell proliferation, differentiation, and inflammation. However, findings on the expression level of HDACs in psoriatic skin lack consistency. We assessed the expression of HDAC1, SIRT1, p63, and proliferating cell nuclear antigen (PCNA) in skin tissues from 23 patients with psoriasis (15 with plaque psoriasis and eight with guttate psoriasis) and five healthy individuals using immunohistochemistry, and analyzed their associations with clinical phenotypes of the disease. The expression of HDAC1 and keratinocyte proliferative markers, such as p63 and PCNA significantly increased, whereas that of SIRT1 decreased in the basal layer (p < 0.05) of the patients with psoriasis compared to those in healthy controls. Among the patients with psoriasis, expression of HDAC1, p63, and PCNA was significantly higher in plaque psoriasis than in guttate psoriasis. There was no significant differences in the level of SIRT1 between the two clinical phenotypes. The findings of this study suggest that histone modifications are involved in the pathogenesis of psoriasis and may contribute to the formation of clinical phenotypes.
Highlights
Psoriasis is a common inflammatory disorder of the skin, characterized by excessive proliferation and abnormal differentiation of keratinocytes [1]
The acetylation of histones is primarily regulated by HDAC1, 2, and 3 proteins, which belong to the class I Histone deacetylases (HDACs) [7]
We examined the expression of HDAC1, sirtuin 1 (SIRT1), and the proliferation markers p63 and proliferating cell nuclear antigen (PCNA) in guttate and plaque psoriasis using immunohistochemistry to investigate whether they are dysregulated in psoriatic skin and if there is any difference between subtypes of psoriasis
Summary
Psoriasis is a common inflammatory disorder of the skin, characterized by excessive proliferation and abnormal differentiation of keratinocytes [1]. Ekman and Enerbӓck found no differences in HDAC activity and HDAC1, 2, and 3 protein expression levels between patients with psoriasis and healthy controls [14]. Similar to HDAC1, SIRT1 removes acetyl groups from histones, but it has various non-histone targets including p53, nuclear factor-κB (NF-κB) and peroxisome proliferator-activated receptor- γ (PPAR-γ) [16]. Only a few studies involving small sample sizes have examined the expression levels of SIRT1 in patients with psoriasis. We examined the expression of HDAC1, SIRT1, and the proliferation markers p63 and proliferating cell nuclear antigen (PCNA) in guttate and plaque psoriasis using immunohistochemistry to investigate whether they are dysregulated in psoriatic skin and if there is any difference between subtypes of psoriasis
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