Dongyin Liu

The Third People's Hospital, Shen-ch’üan-shih, Zhejiang Sheng, China

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Publications (4)11.41 Total impact

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    ABSTRACT: In some skin disorders such as vitiligo and Vogt-Koyanagi-Harada (VKH) syndrome, epidermal melanocytes become the targets of autoimmune response leading to the cell destruction and skin depigmentation. Although CD8+T lymphocytes-mediated autoimmune response is highlighted as the major mechanism of melanocyte destruction in vitiligo and its regulation has been well studied (1, 2), the initial cause that triggers the autoimmune response is still elusive. Scattered vitiligo cases accompanied with viral infection (3) and the discovery of the causative link between viral infection and the vitiligo in animal model (4) implicate the relevance of onset of vitiligo to viruses.This article is protected by copyright. All rights reserved.
    Experimental Dermatology 12/2014; · 4.12 Impact Factor
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    ABSTRACT: Interferon-γ (IFN-γ) plays an important role in the proceedings of vitiligo through recruiting lymphocytes to the lesional skin. However, the potential effects of IFN-γ on skin melanocytes and the subsequent contribution to the vitiligo pathogenesis are still unclear. To investigate the effects of IFN-γ on viability and cellular functions of melanocytes. Primary human melanocytes were treated with IFN-γ. Cell viability, apoptosis, cell cycle melanin content and intracellular reactive oxygen species (ROS) level were measured. mRNA expression was examined by real-time PCR. The release of interleukin 6 (IL-6) and heat shock protein 70 (HSP-70) was monitored by ELISA. β-galactosidase staining was utilized to evaluate melanocyte senescence. Persistent IFN-γ treatment induced viability loss, apoptosis, cell cycle arrest and senescence in melanocytes. Melanocyte senescence was characterized as the changes in pigmentation and morphology, as well as the increase of β-galactosidase activity. Increase of p21Cip1/Waf1 protein was evident in melanocytes after IFN-γ treatment. IFN-γ induction of senescence was attenuated by siRNAs against p21, Janus kinase 2 (JAK2) or signal transducer and activator of transcription 1 (STAT1), but not by JAK1 siRNA nor by p53 inhibitor pifithrin-α. IFN-γ treatment increased the accumulation of intracellular ROS in melanocytes, while ROS scavenger N-acetyl cysteine (NAC) effectively inhibited IFN-γ induced p21 expression and melanocyte senescence. IL-6 and HSP-70 release was significantly induced by IFN-γ treatment, which was largely inhibited by NAC. The increase of IL-6 and HSP-70 release could also be observed in senescent melanocytes. IFN-γ can induce senescence in melanocytes and consequently enhance their immuno-competency, leading to a vitiligo-prone milieu.
    PLoS ONE 01/2014; 9(3):e93232. · 3.53 Impact Factor
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    ABSTRACT: Niacin and its related derivatives have been shown to have effects on cellular activities. However, the molecular mechanism of its reduced immunosuppressive effects and photoprotective effects remains unclear. In this study, we investigated the molecular mechanism of the photoprotective effect of niacin in ultraviolet (UV)-irradiated human skin keratinocytes (HaCaT cells). We found that niacin effectively suppressed the UV-induced cell death and cell apoptosis of HaCaT cells. Existing data have shown that AKT activation is involved in the cell survival process. Yet, the potential mechanism of niacin in protection against UV-induced skin damage has thus far not fully been eluvidated. We observed that niacin pretreatment enhances UV induced activation of AKT (Ser473 phosphorylation) as well as that of the downstream signal mTOR (S6 and 4E-BP1 phosphorylation). The PI3K/AKT inhibitor, LY294002, and the mTOR inhibitor, rapamycin, largely neutralized the protective effects of niacin, suggesting that AKT and downstream signaling mTOR/S6 activation are necessary for the niacin-induced protective effects against UV-induced cell death and cell apoptosis. Collectively, our data suggest that niacin may be utilized to prevent UV-induced skin damage and provide a novel mechanism of its photoprotective effects against the UV radiation of sunlight by modulating both AKT and downstream mTOR signaling pathways.
    International Journal of Molecular Medicine 04/2012; 29(4):593-600. · 1.88 Impact Factor
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    ABSTRACT: Our previous study has shown that VIT1 gene in Chinese vitiligo patients is de facto the FBXO11 gene, and the silencing of that gene has an impact on the ultrastructure of melanocytes. In this study, we further identified the role of the FBXO11 gene in melanocytes and the relationship between dilated endoplasmic reticulum (ER) and tyrosinase by inhibition and overexpression of FBXO11 gene. Cell proliferation, apoptosis, cycle and migration of melanocytes were examined when the FBXO11 gene was silenced or overexpressed. The results showed that FBXO11 gene promoted cell proliferation and suppressed cell apoptosis, and yet had little effect on cell migration. Obvious swelling of ER was found in the cells transfected with siRNA of FBXO11 gene. Interestingly, protein level of tyrosinase was extraordinarily high following inhibition of FBXO11 gene. Further examination revealed that tyrosinase and calreticulin were co-localized in ER of transfected cells following siRNA of FBXO11 gene, suggesting that tyrosinase could not be exported from ER effectively. Collectively, our results support the notion that FBXO11 plays an important role in regulating proliferation and apoptosis of melanocytes, and functional export of tyrosinase from ER in vitiligo melanocytes.
    International Journal of Molecular Medicine 07/2010; 26(1):57-65. · 1.88 Impact Factor