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Differential roles of nitric oxide synthases in regulation of ultraviolet B light-induced apoptosis

Wei Liu1, Shiyong Wu

  • 1Department of Chemistry and Biochemistry, Edison Biotechnology Institute and Molecular and Cellular Biology Program, Ohio University, Athens, OH 45701, USA.

Nitric Oxide : Biology and Chemistry
|June 16, 2010
PubMed

Insights

Ultraviolet B light (UVB) affects nitric oxide (NO) production by NOS enzymes, influencing skin cell apoptosis. This study clarifies the complex roles of constitutive NOSs (cNOSs) and inducible NOS (iNOS) in UVB-induced apoptosis.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Biochemistry

Background:

  • Ultraviolet B (UVB) light exposure can induce apoptosis in skin cells.
  • Nitric oxide (NO) production, regulated by nitric oxide synthases (NOSs), plays a role in apoptosis, but its specific function in UVB-induced apoptosis is debated.
  • Constitutive NOSs (cNOSs) and inducible NOS (iNOS) are key enzymes in NO metabolism.

Purpose of the Study:

  • To investigate the expression and activation of cNOSs and their involvement in UVB-induced apoptosis of HaCaT keratinocytes.
  • To elucidate the dynamic changes in NO and peroxynitrite (ONOO-) levels following UVB exposure.
  • To determine the distinct roles of cNOSs and iNOS in the early and late phases of UVB irradiation.

Main Methods:

  • Analysis of neuronal NOS (nNOS) and endothelial NOS (eNOS) expression and activation in HaCaT cells post-UVB irradiation.
  • Measurement of NO and peroxynitrite (ONOO-) levels at various time points after UVB exposure.
  • Inhibition of cNOS activity using L-NAME to assess its impact on NO/ONOO- balance and apoptosis.

Main Results:

  • UVB increased nNOS expression and uncoupled eNOS early post-irradiation, alongside transient NO elevation and increased ONOO-.
  • iNOS expression increased later, with sustained NO production, while cNOS inhibition altered ONOO- levels differently in early and late phases.
  • Inhibition of cNOSs in the early phase promoted apoptosis via a caspase 3-independent pathway, while contributing to cell protection in the late phase.

Conclusions:

  • cNOSs play a dual role in UVB-induced apoptosis, contributing to NO/ONOO- imbalance and promoting apoptosis early on, but protecting cells later by maintaining a higher NO/ONOO- ratio.
  • The balance between NO and ONOO- regulated by cNOSs is critical in determining the outcome of UVB-induced apoptosis.
  • iNOS becomes the primary source of NO in the later stages of UVB irradiation, influencing cell survival pathways.

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