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Translocator protein ligand Ro5-4864 promotes melanogenesis in a TSPO independent manner
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  • Yunyun Yue,
  • Zi-xian Liao,
  • Yi-chuan Wang,
  • Qiu-yan Liu,
  • Jing Dong,
  • Min Zhong,
  • Ming-han Chen,
  • Yu-min Pan,
  • Hui Zhong,
  • Jing Shang
Yunyun Yue
China Pharmaceutical University

Corresponding Author:[email protected]

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Zi-xian Liao
China Pharmaceutical University
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Yi-chuan Wang
China Pharmaceutical University
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Qiu-yan Liu
China Pharmaceutical University
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Jing Dong
China Pharmaceutical University
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Min Zhong
China Pharmaceutical University
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Ming-han Chen
China Pharmaceutical University
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Yu-min Pan
Guangxi Normal University
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Hui Zhong
China Pharmaceutical University
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Jing Shang
China Pharmaceutical University
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Abstract

The 18-kDa translocator protein (TSPO) is highly conserved among different species but with perplexing biochemical function. Multiple ligands of TSPO show commendable regulatory activities among lots of biological functions, such as neuroinflammation, cholesterol transport and so on. These researches support that TSPO may be a potential target for disease treatment and drug development. Previous studies have shown that its ligand agonist benzodiazepines have the effect of promoting melanin, but the specific mechanism is still unclear. In this research, we firstly confirmed the melanogenesis promotion of Ro5-4864 in mouse melanoma cell line, human skin tissue and zebrafish embryos through inducing melanin synthesis and melanosome transport. Molecular genetics and pharmacological studies showed that TSPO deficiency did not affect melanin production in B16F10 cells and zebrafish embryos, nor did it affect melanin promotion effect of Ro5-4864. The expression of lots of melanogenesis related proteins, such as TYR, TRP-1, DCT, Mlph and Rab27 were upregulated in Ro5-4864 treatment cell with or without Tspo. These results indicated that Ro5-4864 induced melanogenesis in a TSPO independent manner. However, further research is still needed to clarify the direct downstream target of Ro5-4864 in promoting melanogenesis.