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IFN‑γ induces apoptosis in human melanocytes by activating the JAK1/STAT1 signaling pathway

Qianya Su1, Fei Wang1, Zhengbang Dong1

  • 1Department of Dermatology, School of Medicine, Zhong Da Hospital, Southeast University, Nanjing, Jiangsu 210009, P.R. China.

Molecular Medicine Reports
|September 18, 2020
PubMed

Insights

Interferon-gamma (IFN-γ) induces apoptosis in human melanocytes by activating the JAK1/STAT1 pathway. Inhibiting STAT1 reduces this IFN-γ-induced cell death.

Area of Science:

  • Cell Biology
  • Immunology
  • Dermatology

Background:

  • Interferon-gamma (IFN-γ) is a cytokine with diverse biological functions.
  • Melanocytes are crucial skin cells responsible for pigmentation.
  • The JAK/STAT signaling pathway plays a key role in cellular responses to cytokines.

Purpose of the Study:

  • To investigate the role of Janus kinase (JAK)1/Signal transducer and activator of transcription 1 (STAT1) signaling in IFN-γ-induced apoptosis of human melanocytes.
  • To elucidate the molecular mechanisms underlying IFN-γ-mediated melanocyte apoptosis.

Main Methods:

  • Human melanocyte cell cultures were treated with IFN-γ.
  • Cell viability was assessed using Cell Counting Kit-8 assay.
  • Apoptotic rates were determined by flow cytometry.
  • Protein expression and phosphorylation levels (JAK1, JAK2, STAT1, Bcl-2, Bax, Bak, cleaved caspase-3) were analyzed via Western blotting.
  • STAT1 inhibitor (fludarabine) was used to assess pathway dependency.

Main Results:

  • IFN-γ significantly reduced human melanocyte proliferation and induced apoptosis.
  • IFN-γ treatment activated the JAK1/STAT1 signaling pathway.
  • Expression of pro-apoptotic proteins (Bax, Bak, cleaved caspase-3) increased, while anti-apoptotic protein Bcl-2 decreased.
  • Pretreatment with a STAT1 inhibitor attenuated IFN-γ-induced apoptosis.

Conclusions:

  • IFN-γ induces apoptosis in human melanocytes through the activation of the JAK1/STAT1 signaling pathway.
  • This process involves modulation of Bcl-2 family proteins and caspase-3 activation.
  • Targeting the JAK1/STAT1 pathway may offer therapeutic strategies for conditions involving melanocyte apoptosis.

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