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The inhibitory effect of VitD 3 on proliferation of keratinocyte cell line HACAT is mediated by down‐regulation of CXCR2 expression
Author(s) -
Tang L.,
Yu Y.,
Chen J.,
Li Q.,
Yan M.,
Guo Z.
Publication year - 2003
Publication title -
clinical and experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.587
H-Index - 78
eISSN - 1365-2230
pISSN - 0307-6938
DOI - 10.1046/j.1365-2230.2003.01269.x
Subject(s) - hacat , keratinocyte , cxc chemokine receptors , psoriasis , chemokine , cancer research , chemokine receptor , flow cytometry , biology , immunology , interleukin 8 , cell culture , inflammation , genetics
Summary Psoriasis is a disease characterized by inflammation and increased population of hyperproliferative keratinocytes. It is well known that chemokines and chemokine receptors, such as interleukin‐8 and its receptors (CXCR1 and CXCR2), play important roles in the pathogenesis of psoriasis. So far, examination of CXCR2 expression in psoriatic lesional keratinocytes by FACS calibur has not been reported and whether VitD3 inhibits psoriatic lesional keratinocyte proliferation through down‐regulation of CXCR2 expression has not been elucidated. In the present study, CXCR2 expression in psoriatic lesional keratinocytes and HACAT treated with VitD3 was detected by flow cytometry. The proliferative capacity of HACAT treated with VitD3 was assayed by MTT assay. The results showed that CXCR2 expression in psoriatic lesional keratinocytes was higher than that in normal human keratinocytes. At the correct concentration VitD3 could inhibit human keratinocyte proliferation and down‐regulate CXCR2 expression in HACAT. The data demonstrate that the inhibitory effect of VitD3 on keratinocyte proliferation might be mediated by down‐regulation of CXCR2 expression.