ArticlePloS one2014
Interferon-γ induces senescence in normal human melanocytes.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Second Guidelines for the Diagnosis and Treatment of Vitiligo in Japan (2025).The Journal of dermatology · 2026Guideline
- Cytokine-induced senescence in tumors is based on sustained activation of STAT1- and NFκB-dependent gene regulatory signatures.GeroScience · 2026Article
- Dysregulated Intracellular Signaling in the Pathogenesis of Vitiligo: An Update on Emerging Therapeutic Strategies.Biomedicines · 2025Review
- Linking IFN-γ-Mediated Pathogenesis to ROCK-Targeted Therapy in a Scalable iPSCs-Based Vitiligo Model.International journal of molecular sciences · 2025Article
- Ethnicity-specific patterns of epigenetic age acceleration in rheumatoid arthritis.GeroScience · 2025Article
- Cellular senescence promotes macrophage-to-myofibroblast transition in chronic ischemic renal disease.Cell death & disease · 2025Article
- Type-2 immunity associated with type-1 related skin inflammatory diseases: friend or foe?Frontiers in immunology · 2024Review
- Transcriptomic analysis of cellular senescence induced by ectopic expression of ATF6α in human breast cancer cells.PloS one · 2024Article
- Heterogenous Differences in Cellular Senescent Phenotypes in Pre-Eclampsia and IUGR following Quantitative Assessment of Multiple Biomarkers of Senescence.International journal of molecular sciences · 2023Article
- Regenerative Medicine-Based Treatment for Vitiligo: An Overview.Biomedicines · 2022Review
- Stepwise-edited, human melanoma models reveal mutations' effect on tumor and microenvironment.Science (New York, N.Y.) · 2022Article
- Cytokine-Induced Senescence in the Tumor Microenvironment and Its Effects on Anti-Tumor Immune Responses.Cancers · 2022Review
- Article
- Inhibition of Fam114A1 protects melanocytes from apoptosis through higher RACK1 expression.Aging · 2021Article
- Role of Cytokines in Vitiligo: Pathogenesis and Possible Targets for Old and New Treatments.International journal of molecular sciences · 2021Review
- Chronic inflammation-induced senescence impairs immunomodulatory properties of synovial fluid mesenchymal stem cells in rheumatoid arthritis.Stem cell research & therapy · 2021Article
- Human innate immune cell crosstalk induces melanoma cell senescence.Oncoimmunology · 2020Article
- Melanoma Inhibitory Activity (MIA) Is Able to Induce Vitiligo-Like Depigmentation in anFrontiers in medicine · 2020Article
- Tyrosine Kinases in Autoimmune and Inflammatory Skin Diseases.Frontiers in immunology · 2019Review
- Clinical and Molecular Aspects of Vitiligo Treatments.International journal of molecular sciences · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInterferon-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.
objectiveTo investigate the effects of IFN-γ on viability and cellular functions of melanocytes.
methodsPrimary 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.
resultsPersistent 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.
conclusionIFN-γ can induce senescence in melanocytes and consequently enhance their immuno-competency, leading to a vitiligo-prone milieu.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.