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Cited 76 time in webofscience Cited 85 time in scopus
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Whitening effect of adipose-derived stem cells: A critical role of TGF-beta 1

Authors
Kim, WS[Kim, Won-Serk]Park, SH[Park, So-Hyun]Ahn, SJ[Ahn, Se-Jin]Kim, HK[Kim, Hyung-Ki]Park, JS[Park, Jeong-Soo]Lee, GY[Lee, Ga-Young]Kim, KJ[Kim, Kea-Jeung]Whang, KK[Whang, Kyu-Kwang]Kang, SH[Kang, Seung-Hee]Park, BS[Park, Byung-Soon]Sung, JH[Sung, Jong-Hyuk]
Issue Date
Apr-2008
Publisher
PHARMACEUTICAL SOC JAPAN
Keywords
adipose-derived stem cell; melanin; tyrosinase; tyrosinase-related protein 1 (TRP1); transforming growth factor-beta 1
Citation
BIOLOGICAL & PHARMACEUTICAL BULLETIN, v.31, no.4, pp.606 - 610
Indexed
SCIE
SCOPUS
Journal Title
BIOLOGICAL & PHARMACEUTICAL BULLETIN
Volume
31
Number
4
Start Page
606
End Page
610
URI
https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/81767
DOI
10.1248/bpb.31.606
ISSN
0918-6158
Abstract
It has been demonstrated that adipose-derived stem cells (ADSCs) secrete cytokines and exhibit diverse pharmacological actions. The present study examined the unknown pharmacological action of ADSCs regarding whitening effects. A conditioned medium of ADSCs (ADSC-CM) was harvested and the whitening effect of ADSC-CM was studied in melanoma B16 cells. ADSC-CM treatment inhibited the synthesis of melanin and the activity of tyrosinase in a dose dependent manner. To clarify the underlying mechanisms of the whitening action of ADSCs, protein levels of melanogenic proteins were measured by Western blot. Although expressions of microphthalmia-associated transcription factor and tyrosinase-related protein 2 (TRP2) remained unchanged, those of tyrosinase and TRP1 were down-regulated. Transforming growth factor-beta 1 (TGF-beta 1), a potent regulator of melanogenic proteins, was neutralized by the addition of a blocking antibody to ADSC-CM, and down-regulated expression of tyrosinase and TRP1 was almost reversed. Collectively, these results indicate that secretary factors of ADSC inhibit melanin synthesis by down-regulating the expression of tyrosinase and TRP1, which are mainly mediated by TGF-beta 1.
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