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siRNA-mediated knock-down of COX-2 in melanocytes suppresses melanogenesis.

 Ji Y. Kim  ;  Jae Y. Shin  ;  Miri R. Kim  ;  Seung-Kyung Hann  ;  Sang H. Oh 
 EXPERIMENTAL DERMATOLOGY, Vol.21(6) : 420-425, 2012 
Journal Title
Issue Date
Apoptosis ; Cell Line ; Cell Survival ; Cyclooxygenase 2/metabolism* ; Cyclooxygenase 2 Inhibitors/therapeutic use ; Dinoprostone/metabolism ; Gene Knockdown Techniques ; Humans ; Hyperpigmentation/drug therapy ; Interferon Type I/metabolism ; Intramolecular Oxidoreductases/metabolism ; Melanins/biosynthesis* ; Melanocytes/enzymology* ; Melanocytes/pathology ; Microphthalmia-Associated Transcription Factor/metabolism ; Monophenol Monooxygenase/metabolism ; Necrosis ; Pregnancy Proteins/metabolism ; RNA, Small Interfering ; Transfection ; alpha-MSH ; gp100 Melanoma Antigen/metabolism
alpha-melanocyte stimulating hormone ; cyclooxygenase-2 ; melanin ; melanocytes ; siRNA ; tyrosinase
Cyclooxygenase-2 (COX-2) is an enzyme induced in response to multiple mitogenic and inflammatory stimuli, including UV light. UV-induced COX-2 expression induces production of prostaglandin E2 (PGE2) in keratinocytes, which mediates inflammation and cell proliferation. Until recently, studies regarding COX-2 and PGE2 in the skin have focused on keratinocytes and skin cancer and the effect of PGs produced by keratinocytes on melanocytes. However, the effects of COX-2 itself or COX-2 inhibitors on melanogenesis are not well known. Therefore, to establish the role of COX-2 in melanogenesis, we investigated the effects of knock-down of COX-2 in melanocytes on melanin production and the expression of melanogenic molecules through silencing of COX-2 expression with COX-2 short interfering RNA (siRNA). COX-2 knock-down in melanocytes decreased the expressions of tyrosinase, TRP-1, TRP-2, gp100 and MITF and also reduced tyrosinase enzyme activity. Furthermore, COX-2 siRNA-transfected melanocytes showed markedly reduced alpha-melanocyte stimulating hormone (α-MSH)-induced melanin production. In addition, α-MSH-induced COX-2 expression in both scrambled siRNA-transfected and COX-2 siRNA-transfected melanocytes was greater than α-MSH-untreated cells. Our results suggest that COX-2 might be a candidate target for the development of anti-melanogenic agents and α-MSH-induced pigmentation could be closely associated with COX-2 expression. COX-2 inhibitors might therefore be of particular use in whitening cosmetics for hyperpigmentation disorders such as melasma, postinflammatory hyperpigmentation and solar lentigo.
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1. College of Medicine (의과대학) > Dept. of Dermatology (피부과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Miri(김미리)
Shin, Jae Yong(신재용)
Oh, Sang Ho(오상호) ORCID logo https://orcid.org/0000-0002-4477-1400
Hann, Seung Kyung(한승경)
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