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Updated: May 1, 2026
Techniques to Induce and Quantify Cellular Senescence
Published on: May 1, 2017
Interferon-γ induces senescence in normal human melanocytes
Suiquan Wang1, Miaoni Zhou1, Fuquan Lin1
1Department of Dermatology, Hangzhou Institute of Dermatology and Venereology, Third People's Hospital of Hangzhou, Hangzhou, Zhejiang Province, China.
Insights
Interferon-γ (IFN-γ) induces melanocyte senescence, impacting skin immunity and contributing to vitiligo. This process involves reactive oxygen species (ROS) and the p21 protein, highlighting new therapeutic targets.
Area of Science:
- Dermatology
- Immunology
- Cell Biology
Background:
- Interferon-γ (IFN-γ) is implicated in vitiligo pathogenesis by recruiting lymphocytes.
- The specific effects of IFN-γ on skin melanocytes remain largely unknown.
Purpose of the Study:
- To investigate the impact of IFN-γ on melanocyte viability and function.
- To elucidate the mechanisms underlying IFN-γ-induced melanocyte alterations.
Main Methods:
- Primary human melanocytes were exposed to IFN-γ.
- Assessed were cell viability, apoptosis, cell cycle, melanin content, and reactive oxygen species (ROS).
- Senescence was evaluated using β-galactosidase staining, with molecular markers like p21 analyzed via real-time PCR and protein assays.
Main Results:
- IFN-γ induced melanocyte senescence, characterized by reduced viability, apoptosis, cell cycle arrest, and increased β-galactosidase activity.
- Senescence was mediated by p21, JAK2, and STAT1 signaling pathways, and significantly influenced by ROS accumulation.
- IFN-γ stimulated the release of IL-6 and HSP-70, which was mitigated by ROS inhibition.
Conclusions:
- IFN-γ triggers melanocyte senescence, enhancing their immune-competency.
- This IFN-γ-induced senescence contributes to a pro-inflammatory environment, promoting vitiligo development.
Background:
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.
Objective:
To investigate the effects of IFN-γ on viability and cellular functions of melanocytes.
Methods:
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.
Results:
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.
Conclusion:
IFN-γ can induce senescence in melanocytes and consequently enhance their immuno-competency, leading to a vitiligo-prone milieu.
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