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2000
Volume 28, Issue 4
  • ISSN: 1386-2073
  • E-ISSN: 1875-5402

Abstract

Background

Vitiligo is an autoimmune skin disorder primarily characterized by the absence of melanocytes, leading to the development of white patches on the patient's skin. Narrowband Ultraviolet B (NB-UVB) therapy is among the most effective approaches for stimulating the reformation of hyperpigmentation. This treatment utilizes a narrow spectrum of NB-UVB wavelengths ranging from 311 to 313 nm to irradiate the affected area, thereby preventing the destruction of migrating and proliferating melanocytes. Nevertheless, the molecular alterations occurring in both the hair follicle and the interfollicular epidermis during NB-UVB treatment remain unknown.

Methods

In this study, we conducted a comprehensive analysis of the consistency of differentially expressed genes (DEGs) within the enrichment pathways both before and after NB-UVB treatment, utilizing a bioinformatics approach. Furthermore, we employed CYTOHUBBA and Random Forest algorithms to identify and sequence hub genes from the pool of DEGs. Following validation of these hub genes through ROC curve analysis, we proceeded to construct an interaction network between these hub genes, miRNA, and drugs. Real-Time Quantitative Polymerase Chain Reaction (RT-qPCR) was used to further verify the difference in the expression of hub genes between the disease group and the control group.

Results

Gene Set Enrichment Analysis of DEGs indicated strong associations with vitiligo in most pathways. Subsequently, we conducted Gene Ontology and Metascape enrichment analyses on the overlapping genes from DEGs. We identified key genes (COL11A1, IGFBP7, LOX, NTRK2, SDC2, SEMA4D, and VEGFA) within the Protein-Protein Interaction (PPI) network. We further explored potential drugs that could be used for the clinical treatment of vitiligo through the drug-hub gene interaction network. Finally, the results of RT-qPCR experiments demonstrated that the expression levels of the identified hub genes in both groups were consistent with the bioinformatics analysis results.

Conclusion

The hub genes obtained in this study may be a biomarker related to the development of vitiligo pigmentation. Our research not only contributes to a better understanding of the treatment mechanisms of vitiligo but also provides valuable insights for future personalized medical approaches and targeted therapies for vitiligo.

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References

  1. KrügerC. SchallreuterK.U. A review of the worldwide prevalence of vitiligo in children/adolescents and adults.Int. J. Dermatol.201251101206121210.1111/j.1365‑4632.2011.05377.x 22458952
    [Google Scholar]
  2. DiotalleviF. GioacchiniH. De SimoniE. MaraniA. CandeloraM. PaolinelliM. MolinelliE. OffidaniA. SimonettiO. Vitiligo, from pathogenesis to therapeutic advances: State of the art.Int. J. Mol. Sci.2023245491010.3390/ijms24054910 36902341
    [Google Scholar]
  3. IwanowskiT. KołkowskiK. NowickiR.J. Sokołowska-WojdyłoM. Etiopathogenesis and emerging methods for treatment of vitiligo.Int. J. Mol. Sci.20232411974910.3390/ijms24119749 37298700
    [Google Scholar]
  4. AmerA. WuY. LiC. DuJ. JiaH. LiS. TuC. LiQ. LiuH. ZhangJ. LuT. LiuJ. MeiA. LiuH. TianF. LuC. LiZ. CaoL. GaoX. Burden of vitiligo on Chinese patients: An online survey.Chin. Med. J.2023136192365236710.1097/CM9.0000000000002429 36805553
    [Google Scholar]
  5. RodriguesM. EzzedineK. HamzaviI. PandyaA.G. HarrisJ.E. New discoveries in the pathogenesis and classification of vitiligo.J. Am. Acad. Dermatol.201777111310.1016/j.jaad.2016.10.048 28619550
    [Google Scholar]
  6. EzzedineK. EleftheriadouV. WhittonM. van GeelN. Vitiligo.Lancet20153869988748410.1016/S0140‑6736(14)60763‑7 25596811
    [Google Scholar]
  7. YuanX. MengD. CaoP. SunL. PangY. LiY. WangX. LuoZ. ZhangL. LiuG. Identification of pathogenic genes and transcription factors in vitiligo.Dermatol. Ther.2019325e1302510.1111/dth.13025 31306558
    [Google Scholar]
  8. BonifaceK. JacqueminC. DarrigadeA.S. DessartheB. MartinsC. BoukhedouniN. VernisseC. GrasseauA. ThiolatD. RambertJ. LuccheseF. BertolottiA. EzzedineK. TaiebA. SeneschalJ. Vitiligo skin is imprinted with resident memory CD8 T cells expressing CXCR3.J. Invest. Dermatol.2018138235536410.1016/j.jid.2017.08.038 28927891
    [Google Scholar]
  9. Bouceiro MendesR. AlpalhãoM. FilipeP. UVB phototherapy in the treatment of vitiligo: State of the art and clinical perspectives.Photodermatol. Photoimmunol. Photomed.202238321522310.1111/phpp.12740 34626483
    [Google Scholar]
  10. KhaitanB.K. BhatiaS. GuptaV. KhandpurS. SahniK. SreenivasV. Efficacy of NB-UVB in progressive versus non-progressive non-segmental vitiligo: A prospective comparative study.Indian Dermatol. Online J.202112570170510.4103/idoj.IDOJ_40_21 34667756
    [Google Scholar]
  11. YuanX. WangL. MengD. WuL. WangX. ZhangD. LuoZ. PangY. LiuG. The impact of NBUVB on microbial community profiling in the lesional skin of vitiligo subjects.Microb. Pathog.202014010394310.1016/j.micpath.2019.103943 31917273
    [Google Scholar]
  12. DongB.Q. LiaoZ.K. LeY. JiangS. LuoL.F. MiaoF. Le PooleI.C. LeiT.C. Acceleration of melanocyte senescence by the proinflammatory cytokines IFNγ and TNFα impairs the repigmentation response of vitiligo patients to narrowband ultraviolet B (NBUVB) phototherapy.Mech. Ageing Dev.202321111177910.1016/j.mad.2023.111779 36731753
    [Google Scholar]
  13. LoganathanL. KuriakoseB.B. MushfiqS. MuthusamyK. Mechanistic insights on nsSNPs on binding site of renin and cytochrome P450 proteins: A computational perceptual study for pharmacogenomics evaluation.J. Cell. Biochem.2021122101460147410.1002/jcb.30069 34161641
    [Google Scholar]
  14. RenH. WangG. JiangJ. LiJ. FuL. LiuL. LiN. ZhaoJ. SunX. ZhangL. ZhangH. ZhouP. Comparative transcriptome and histological analyses provide insights into the prenatal skin pigmentation in goat (Capra hircus).Physiol. Genomics2017491270371110.1152/physiolgenomics.00072.2017 28972038
    [Google Scholar]
  15. LiaoY.H. HuangY.T. DengJ.Y. ChenW.S. JeeS.H. Pulsed ultrasound promotes melanoblast migration through upregulation of macrophage colony‐stimulating factor/focal adhesion kinase autocrine signaling and paracrine mechanisms.Pigment Cell Melanoma Res.201326565466510.1111/pcmr.12125 23725022
    [Google Scholar]
  16. KimJ.H. HongA. KimY.H. YooH. KangS.W. ChangS.E. SongY. JNK suppresses melanogenesis by interfering with CREB-regulated transcription coactivator 3-dependent MITF expression.Theranostics20201094017402910.7150/thno.41502 32226536
    [Google Scholar]
  17. NataleC.A. DuperretE.K. ZhangJ. SadeghiR. DahalA. O’BrienK.T. CooksonR. WinklerJ.D. RidkyT.W. Sex steroids regulate skin pigmentation through nonclassical membrane-bound receptors.eLife20165e1510410.7554/eLife.15104 27115344
    [Google Scholar]
  18. HanH. KimY. MoH. ChoiS.H. LeeK. RimY.A. JuJ.H. Preferential stimulation of melanocytes by M2 macrophages to produce melanin through vascular endothelial growth factor.Sci. Rep.2022121641610.1038/s41598‑022‑08163‑7 35440608
    [Google Scholar]
  19. KangB. KimY. ParkT.J. KangH.Y. Dasatinib, a second-generation tyrosine kinase inhibitor, induces melanogenesis via ERK-CREB-MITF-tyrosinase signaling in normal human melanocytes.Biochem. Biophys. Res. Commun.202052341034103910.1016/j.bbrc.2020.01.051 31973810
    [Google Scholar]
  20. LyuY. TschulakowA.V. WangK. BrashD.E. SchraermeyerU. Chemiexcitation and melanin in photoreceptor disc turnover and prevention of macular degeneration.Proc. Natl. Acad. Sci. USA202312020e221693512010.1073/pnas.2216935120 37155898
    [Google Scholar]
  21. GottesbergeA.M.M.E.Y.E.R. Physiology and pathophysiology of inner ear melanin.Pigment Cell Res.19881423824910.1111/j.1600‑0749.1988.tb00422.x 3070525
    [Google Scholar]
  22. ChenL. WangL. ChenL. WangF. JiF. SunW. ZhaoH. HanW. YangS. Transcript profiles of stria vascularis in models of waardenburg syndrome.Neural Plast.202020201910.1155/2020/2908182 32802035
    [Google Scholar]
  23. BelleiB. PitisciA. OttavianiM. LudoviciM. CotaC. LuziF. Dell’AnnaM.L. PicardoM. Vitiligo: A possible model of degenerative diseases.PLoS One201383e5978210.1371/journal.pone.0059782 23555779
    [Google Scholar]
  24. JungH. ChungH. ChangS.E. ChoiS. HanI.O. KangD.H. OhE.S. Syndecan‐2 regulates melanin synthesis via protein kinase C βII ‐mediated tyrosinase activation.Pigment Cell Melanoma Res.201427338739710.1111/pcmr.12223 24472179
    [Google Scholar]
  25. AminiF. Thazin OoN.M. OkechukwuP.N. SeghayatM.S. NgE.S.C. Polymorphisms in P53 and VEGFA genes in different subtypes of periorbital hyperpigmentation in a Malaysian Chinese population.Australas. J. Dermatol.2019602e99e10410.1111/ajd.12918 30215845
    [Google Scholar]
  26. KimK.I. JungK.E. ShinY.B. KimC.D. YoonT.J. Sorafenib induces pigmentation via the regulation of β‐catenin signalling pathway in melanoma cells.Exp. Dermatol.2022311576310.1111/exd.14112 32391926
    [Google Scholar]
  27. WeiB. ZhangY.P. YanH.Z. XuY. DuT.M. Cilostazol promotes production of melanin by activating the microphthalmia-associated transcription factor (MITF).Biochem. Biophys. Res. Commun.2014443261762110.1016/j.bbrc.2013.12.017 24333333
    [Google Scholar]
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  • Article Type:
    Research Article
Keyword(s): biomarker; hub genes; NB-UVB therapy; PPI; RT-qPCR; Vitiligo
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