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Neural stem cells inhibit melanin production by activation of Wnt inhibitors

Insik Hwang1, Ju-Hwang Park, Hang-Soo Park

  • 1Laboratory of Stem Cell Biology, Department of Biomedical Science, College of Health Science, Korea University, Jeongneung-dong, Sungbuk-gu, Seoul 136-703, Republic of Korea; Department of Health Science, Korea University Graduate School, Jeongneung-dong, Sungbuk-gu, Seoul 136-703, Republic of Korea.

Journal of Dermatological Science
|September 11, 2013
PubMed
Abstract

Insights

Human neural stem cell-conditioned medium (NSC-CM) effectively inhibits melanin production in melanoma cells and mice. This effect is mediated by the downregulation of key pigmentation enzymes and the Wnt/β-catenin signaling pathway.

Area of Science:

  • Dermatology
  • Cell Biology
  • Stem Cell Research

Background:

  • Melanin synthesis is regulated by tyrosinase (TYR), TRP1, and DCT/TRP2, controlled by microphthalmia-associated transcription factor (MITF).
  • MITF is a key regulator of pigmentation and a target of Wnt/β-catenin signaling during melanocyte differentiation.
  • The mechanisms of conditioned medium (CM)-mediated effects on skin pigmentation are not fully understood.

Purpose of the Study:

  • To investigate the inhibitory effects and mechanisms of human neural stem cell-conditioned medium (NSC-CM) on melanin synthesis.
  • To elucidate the role of NSC-CM in B16 melanoma cells and UV-B irradiated C57/BL-6 mice.

Main Methods:

  • B16-F10 melanoma cells and mouse skin were treated with varying concentrations of NSC-CM.
  • Melanin content and tyrosinase activity were measured.
  • Gene and protein expression of key pigmentation factors (TYR, TRP1, DCT/TRP2, MITF, β-catenin) and Wnt inhibitors were analyzed using RT-PCR and Western blot.

Main Results:

  • NSC-CM significantly reduced melanin content and the expression of TYR, TRP1, DCT/TRP2, MITF, and β-catenin in both cell and animal models.
  • NSC-CM suppressed Wnt/β-catenin signaling by decreasing β-catenin expression.
  • This suppression was attributed to increased expression of Wnt inhibitors Dickkopf-1 (DKK1) and secreted frizzled-related protein 2 (sFRP2).

Conclusions:

  • NSC-CM effectively suppresses melanin production in vitro and in vivo.
  • Factors within NSC-CM play a significant role in regulating epidermal melanogenesis.
  • NSC-CM demonstrates potential for therapeutic applications in pigmentation disorders.
Keywords:
(2′Z, 3′E)-6-bromoindirubin-3′-oximeAPCBIOCK1αDKK1,2,3Dct/TRP2Dickkopf-1,2,3DishevelledDvlGSK-3βMITFMelaninNSC culture mediumNSC-CMNeural stem cell-conditioned mediumPMSFSCFT-cell factor/lymphoid enhancer factorTCF/LEFTRP1TYRTyrosinaseWIF1Wnt inhibitorsWnt inhibitory factor1adenomatous polyposis colicasein kinase1αdopachrome tautomerase/tyrosinase related protein 2glycogen synthase kinase 3βmicrophthalmia-associated transcription factorneural stem cell conditioned mediumnon-CMphenylmethyl sulfonyl fluoridesFRP1,2,4,5secreted frizzled-related proteinstem cell factortyrosinasetyrosinase-related protein 1α-MSHα-melanocyte-stimulating hormone

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