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Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response
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Prostacyclin: an inflammatory paradox.

Jeremiah Stitham1, Charles Midgett, Kathleen A Martin

  • 1Section of Cardiovascular Medicine, Department of Internal Medicine, Yale School of Medicine, Yale University New Haven, CT, USA.

Frontiers in Pharmacology
|June 21, 2011
PubMed
Summary

Prostacyclin (PGI(2)) acts as both a pro-inflammatory mediator in rheumatoid arthritis and an anti-inflammatory agent in pulmonary vascular disease and atherosclerosis. This review explores its dual role in inflammatory diseases and therapeutic potential.

Keywords:
IP receptoratherosclerosisinflammationprostacyclinpulmonary fibrosisrheumatoid arthritis

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Area of Science:

  • Biochemistry
  • Immunology
  • Cardiovascular Biology

Background:

  • Prostacyclin (PGI(2)), a bioactive lipid, is primarily known for its cardiovascular functions, including vasodilation and inhibition of platelet aggregation.
  • Beyond cardiovascular roles, PGI(2) influences vascular smooth muscle cell differentiation and proliferation.
  • Emerging evidence highlights PGI(2)'s significant involvement as an inflammatory mediator in various disease processes.

Purpose of the Study:

  • To review the dual role of prostacyclin (PGI(2)) as a pathophysiological mediator and therapeutic agent in inflammatory diseases.
  • To examine PGI(2)'s pro-inflammatory contribution in rheumatoid arthritis.
  • To analyze PGI(2)'s anti-inflammatory role in pulmonary vascular disease and atherosclerosis.

Main Methods:

  • This study is a review of existing literature on prostacyclin (PGI(2)) in inflammatory diseases.
  • The review synthesizes findings on PGI(2)'s mechanisms in rheumatoid arthritis, pulmonary vascular disease, and atherosclerosis.
  • Focus is placed on PGI(2)'s impact on disease progression and its therapeutic implications.

Main Results:

  • Prostacyclin (PGI(2)) acts as a pro-inflammatory mediator, promoting disease progression in rheumatoid arthritis.
  • Conversely, PGI(2) functions as an anti-inflammatory agent, inhibiting disease progression in pulmonary vascular disease and atherosclerosis.
  • PGI(2) demonstrates a complex, context-dependent role in inflammatory conditions.

Conclusions:

  • Prostacyclin (PGI(2)) exhibits a dichotomous role in inflammatory diseases, acting as both a promoter and inhibitor of disease progression.
  • Understanding PGI(2)'s complex molecular basis is crucial for elucidating inflammatory disease mechanisms.
  • The findings offer insights into developing current and future anti-inflammatory treatments targeting PGI(2) pathways.