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

Ji Y. Kim, Jae Y. Shin, Miri R. Kim, Seung Kyung Hann, SangHo Oh

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)420-425
Number of pages6
JournalExperimental dermatology
Volume21
Issue number6
DOIs
Publication statusPublished - 2012 Jun 1

Fingerprint

Melanocytes
Cyclooxygenase 2
Small Interfering RNA
Melanocyte-Stimulating Hormones
Keratinocytes
Hyperpigmentation
Monophenol Monooxygenase
Cyclooxygenase 2 Inhibitors
Melanins
Dinoprostone
Skin
Lentigo
Melanosis
alpha-MSH
Cosmetics
Pigmentation
Cell proliferation
Enzyme activity
Skin Neoplasms
Enzymes

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Dermatology

Cite this

Kim, Ji Y. ; Shin, Jae Y. ; Kim, Miri R. ; Hann, Seung Kyung ; Oh, SangHo. / siRNA-mediated knock-down of COX-2 in melanocytes suppresses melanogenesis. In: Experimental dermatology. 2012 ; Vol. 21, No. 6. pp. 420-425.
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siRNA-mediated knock-down of COX-2 in melanocytes suppresses melanogenesis. / Kim, Ji Y.; Shin, Jae Y.; Kim, Miri R.; Hann, Seung Kyung; Oh, SangHo.

In: Experimental dermatology, Vol. 21, No. 6, 01.06.2012, p. 420-425.

Research output: Contribution to journalArticle

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AU - Shin, Jae Y.

AU - Kim, Miri R.

AU - Hann, Seung Kyung

AU - Oh, SangHo

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AB - 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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