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Related Experiment Videos

Inflammatory modulation of PPAR gamma expression and activity.

Michelle B Crosby1, John Zhang, Tamara M Nowling

  • 1Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USA.

Clinical Immunology (Orlando, Fla.)
|November 24, 2005
PubMed
Summary

In lupus-prone mice, increased nitric oxide (NO) production correlates with disease. Reduced peroxisome proliferation activated receptor gamma (PPARgamma) activity may worsen this, suggesting a new therapeutic target.

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Area of Science:

  • Immunology
  • Nephrology
  • Molecular Biology

Background:

  • Nitric oxide (NO) production escalates with age in lupus-prone MRL/lpr mice, mirroring disease progression.
  • Dysregulation of the inducible nitric oxide synthase (iNOS) pathway may contribute to excess NO production.
  • Peroxisome proliferation activated receptor gamma (PPARgamma), a nuclear hormone receptor, is a potential modulator of NO.

Purpose of the Study:

  • To investigate the role of PPARgamma in regulating NO production in MRL/lpr mice.
  • To determine if PPARgamma expression and activity are altered during lupus progression.
  • To explore the relationship between inflammatory mediators, PPARgamma, and NO production in mesangial cells.

Main Methods:

  • Assessed renal PPARgamma and iNOS protein expression in MRL/lpr mice at different disease stages.

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  • Compared PPARgamma expression and NO production in primary mesangial cells from MRL/lpr and BALB/c mice.
  • Evaluated the impact of inflammatory mediators and a NOS inhibitor on PPARgamma activity in mesangial cells.

    • Main Results:

    • Renal PPARgamma protein expression decreased as disease progressed in MRL/lpr mice, correlating with increased iNOS protein.
    • MRL/lpr mesangial cells exhibited lower PPARgamma expression and higher NO production compared to BALB/c cells.
    • Exposure to inflammatory mediators reduced PPARgamma activity in mesangial cells, which was restored by a NOS inhibitor.

    Conclusions:

    • Inflammatory pathways in lupus may reduce PPARgamma activity and expression.
    • This reduction in PPARgamma exacerbates NO production and disease severity.
    • PPARgamma represents a potential therapeutic target for managing NO-related complications in lupus.