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• Research Paper Volume 13, Issue 4 pp 5415-5425

  A retrospective study of long term follow-up of 2283 vitiligo patients treated by autologous, non-cultured melanocyte–keratinocyte transplantation

  Relevance score: 8.055986

  Dimin Zhang, Xiaodong Wei, Weisong Hong, Lifang Fu, Guopei Qian, Ai-e Xu

  Keywords: vitiligo, non-cultured melanocyte-keratinocyte transplantation

  Published in Aging on February 11, 2021

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  Background: Autologous non-cultured melanocyte-keratinocyte transplantation (MKTP) can be used to treat stable vitiligo cases, but there were insufficient clinical data to evaluate its safety and efficacy.

  Objective: To assess the influence of various factors on the therapeutic outcome of MKTP.

  Method: The single-center retrospective study included stable vitiligo patients who underwent MKTP between June 2009 and June 2018. Univariate and/or multivariable analysis were used to determine the factors affecting the outcome of repigmentation.

  Result: The study comprised 2283 patients who had long-term follow-up data (12-108months). Excellent repigmentation was achieved in 400/606 (66%),788/1341 (58.8%),437/684 (63.9%),18/24 (75%) patients with segmental vitiligo, pre-MKTP phototherapy, younger than 24 years, the lesion on the perineum and scrotum, respectively. However, the patients with a positive family history, Koebner phenomenon responded worse(χ²=29.417, P<0.001; χ²=107.397, P<0.001; respectively). Overall, a significant positive correlation between duration of stability and percentage of repigmentation was found (χ²=42.053, P<0. 001).

  Conclusion: MKTP is efficient and well tolerated for stable vitiligo treatment. Various factors such as duration of disease stability, vitiligo type, family history, site of lesion should be carefully assessed before using MKTP, as it would further improve the post-operative repigmentation.

• Research Paper Volume 11, Issue 24 pp 11829-11843

  Suppression of FADS1 induces ROS generation, cell cycle arrest, and apoptosis in melanocytes: implications for vitiligo

  Relevance score: 7.325934

  Luyan Tang, Jian Li, Wenwen Fu, Wenyu Wu, Jinhua Xu

  Keywords: vitiligo, microarray, fatty acid desaturase 1, apoptosis, melanocyte

  Published in Aging on December 21, 2019

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  Vitiligo is a potentially serious condition characterized by loss of melanin and death of melanocytes. To identify potential therapeutic targets for vitiligo, we conducted a microarray analysis of three human vitiligo specimens and paired adjacent normal tissues. Because we found that the fatty acid desaturase 1 (FADS1) gene was downregulated in vitiligo specimens, we carried out experiments to assess its role in melanocyte replication and survival. RT-qPCR was used to verify that FADS1 expression was lower in vitiligo-affected tissues and vitiligo melanocyte PIG3V cells than in matched controls or normal human epidermal PIG1 melanocytes. In addition, CCK-8, immunofluorescence, western blot and flow cytometry assay were used to detect the proliferation and apoptosis in PIG1 cells respectively. Overexpression of FADS1 promoted proliferation of PIG3V melanocytes, while FADS1 silencing inhibited proliferation and induced cell death in PIG1 melanocytes. Increased ROS generation; induction of mitochondrial-mediated apoptosis via upregulation of Bax and active caspases 3 and 9 and downregulation of Bcl-2; and cell cycle arrest via downregulation of c-Myc and Cyclin D1 and upregulation of p21 were all enhanced after FADS1 silencing in PIG1 melanocytes. These findings implicate FADS1 downregulation in the pathogenesis of vitiligo and may open new avenues for its treatment.

  

  Differential gene expression analysis in clinical vitiligo specimens. (A) Heat map showing gene expression profiles in clinical samples of vitiligo and matched, adjacent normal specimens; each column represents one sample. Red and green indicate upregulation and downregulation, respectively. (B) Distribution of gene transcripts presented as MA plot (log2 fold-change vs log total counts); red points indicate DEGs (FADS1, log2 fold-change = -3.82, -log10 (p-value) = 2.84). (C) Gene ontology (GO) enrichment analysis of DEGs. (D) Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis of DEGs. N1, N2, N3: normal specimens; P1, P2, P3: vitiligo samples.

  
  
  

  

  Expression of FADS1 in human vitiligo specimens and melanocyte cell lines. (A) Relative expression of FADS1, HACD2, and ELOVL5 in vitiligo samples (P) and matched normal tissues (N) by qRT-PCR (n = 9). (B) Free fatty acid in vitiligo samples (P) and matched normal tissues (N) detected by ELISA kit. (C) FADS1 expression in the vitiligo melanocyte cell line PIG3V and in the normal epidermal melanocyte cell line PIG1 detected by qRT-PCR. (D) FADS1 expression by qRT-PCR in PIG1 cells transfected with NC-siRNA, FADS1-siRNA1, or FADS1-siRNA2 for 72 h. (E) FADS1 expression by qRT-PCR in PIG3V in cells transfected with lenti-NC or lenti-FADS1 for 72 h. **P < 0.01, compared with NC cells.

  
  
  

  

  Overexpression of FADS1 promotes proliferation of PIG3V melanocytes. PIG3V cells were transduced with lenti-NC or lenti-FADS1 for 72 h. (A) Cell viability determination (CCK-8 assay). (B, C) Ki67 immunofluorescence. (D, E) Western blot detection of FADS1. **P < 0.01, compared with the NC group.

  
  
  

  

  Downregulation of FADS1 induces apoptosis in PIG1 melanocytes. PIG1 cells were transfected with NC-siRNA or FADS1-siRNA2 for 72 h. (A) Cell viability determination (CCK-8 assay). (B, C) Ki67 immunofluorescence. (D, E) Cell death (trypan blue) assay. (F, G) Apoptosis assay. Annexin V/PI-stained cells were analyzed by flow cytometry. (H, I) Expression of FADS1 by western blot. **P < 0.01, compared with NC cells.

  
  
  

  

  Downregulation of FADS1 decreased melanogenesis in PIG1 melanocytes. PIG1 cells were transfected with NC-siRNA or FADS1-siRNA2 for 72 h. (A) Melanin content determination (ELISA). (B) Expression of MITF, Tyrosinase, TRP1, and TRP2 detected by western blotting. β-actin was used as internal control. (C–F) Relative expression of MITF, Tyrosinase, TRP1, and TRP2 after normalization to β-actin. **P < 0.01, compared with NC cells.

  
  
  

  

  Downregulation of FADS1 induces ROS generation, decreases MMP, and promotes expression of apoptosis markers in PIG1 cells. PIG1 melanocytes were transfected with NC-siRNA or FADS1-siRNA2 for 24 h or 72 h. (A, B) ROS generation measured by DCF fluorescence using flow cytometry. (C) Changes in MMP assessed through JC-1 staining and flow cytometry. (D) The ultrastructural morphological changes of mitochondria in PIG1 cells observed on the TEM. (E) Expression of Bax, Bcl-2, active caspase 9, and active caspase 3 detected by western blotting. β-actin was used as internal control. (F–I) Relative expression of Bax, Bcl-2, active caspase 9, and active caspase 3 after normalization to β-actin. **P < 0.01, compared with NC cells.

  
  
  

  

  Downregulation of FADS1 inhibits cell cycle progression in PIG1 melanocytes. PIG1 cells were transfected with NC-siRNA or FADS1-siRNA2 for 72 h. (A, B) Cell cycle staging measured by flow cytometry. (C) Western blot detection of c-Myc, p21, and Cyclin D1 expression. β-actin was used as internal control. (D–F) Relative expression of c-Myc, p21, and Cyclin D1 after normalization to β-actin. **P < 0.01, compared with the NC group.

  
  
  

  

  Downregulation of FADS1 inhibited melanogenesis by inhibiting the MAPK signaling pathway. PIG1 cells were transfected with NC-siRNA or FADS1-siRNA2 for 72 h. (A) Western blot detection of p-p38 and p-JNK expression. β-actin was used as internal control. (B, C) Relative expression of p-p38 and p-JNK after normalization to p38 and JNK. **P < 0.01, compared with the NC group.

  
  
  

  

  Schematic model of apoptotic melanocyte death mediated by FADS1 downregulation. Downregulation of FADS1 increases reactive oxygen species (ROS) generation, which led to inhibition of the p38/ERK MAPK signaling pathway. Furthermore, Downregulation of FADS1 induces apoptosis and cell cycle arrest in PIG1 cells via inhibition of the p38/ERK MAPK signaling pathway.