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A Method to Study the C924T Polymorphism of the Thromboxane A2 Receptor Gene
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Atf3 negatively regulates Ptgs2/Cox2 expression during acute inflammation.

Jason Hellmann1, Yunan Tang2, Michael J Zhang2

  • 1Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Harvard Institutes of Medicine, Boston, MA 02115, United States.

Prostaglandins & Other Lipid Mediators
|January 27, 2015
PubMed
Summary

Activating transcription factor-3 (Atf3) suppresses cyclooxygenase-2 (Cox-2/Ptgs2) during inflammation. Loss of Atf3 increases inflammatory mediators, suggesting Atf3 is a therapeutic target.

Keywords:
InflammationLipid mediatorsProstaglandins

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Area of Science:

  • Immunology
  • Molecular Biology
  • Inflammation Research

Background:

  • Cyclooxygenase-2 (Cox-2/Ptgs2) generates prostaglandins crucial for inflammatory responses.
  • Mechanisms regulating the termination of Ptgs2 gene transcription remain incompletely understood.

Purpose of the Study:

  • To investigate the role of activating transcription factor-3 (Atf3) in regulating Ptgs2 expression during inflammation.
  • To explore the potential of the Atf3-Ptgs2 axis as a therapeutic target for inflammatory diseases.

Main Methods:

  • Macrophage stimulation with yeast zymosan.
  • Quantitative analysis of Ptgs2 and Atf3 expression in wild-type and Atf3 knockout mice.
  • Chromatin-immunoprecipitation assays to assess Atf3 binding to the Ptgs2 promoter.
  • Assessment of inflammatory responses in vivo using models of acute peritonitis and cutaneous wounds.

Main Results:

  • Zymosan stimulation induced transient Ptgs2 expression alongside increased Atf3 expression in macrophages.
  • Ptgs2 expression and prostaglandin production were elevated in Atf3(-/-) macrophages.
  • Atf3 was recruited to the Ptgs2 promoter region in activated macrophages.
  • Atf3(-/-) mice exhibited increased leukocyte accumulation and prostaglandin levels in inflammatory exudates.

Conclusions:

  • Atf3 acts as a negative regulator of Ptgs2 during acute inflammation.
  • Dysregulation of the Atf3-Ptgs2 axis may contribute to chronic inflammatory conditions.
  • Targeting the Atf3-Ptgs2 pathway offers a potential therapeutic strategy for suppressing inflammation.