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Related Experiment Videos

Cyclooxygenases, microsomal prostaglandin E synthase-1, and cardiovascular function.

Yan Cheng1, Miao Wang, Ying Yu

  • 1Institute for Translational Medicine and Therapeutics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.

The Journal of Clinical Investigation
|April 15, 2006
PubMed
Summary

Inhibitors of COX-2 increase cardiovascular risks by suppressing prostacyclin (PGI(2)) and PGE(2). Targeting microsomal PGE synthase-1 (mPGES-1) may offer anti-inflammatory benefits without these adverse effects.

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Area of Science:

  • Biochemistry
  • Pharmacology
  • Cardiovascular Research

Background:

  • Prostaglandin G/H synthase-2 (PGHS-2/COX-2) inhibitors are linked to increased myocardial infarction and stroke.
  • Adverse cardiovascular events are associated with the suppression of PGHS-2-derived prostacyclin (PGI(2)) and PGE(2).

Purpose of the Study:

  • To investigate mechanisms underlying COX-2 inhibitor-induced cardiovascular events.
  • To identify therapeutic targets that suppress inflammatory mediators while avoiding cardiovascular risks.

Main Methods:

  • Selective inhibition, knockout, or mutation of PGHS-2 in mice.
  • Deletion of the PGI(2) receptor in mice.
  • COX-1 knockdown in mice.
  • Deletion of microsomal PGE synthase-1 (mPGES-1) in mice.

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Main Results:

  • PGHS-2 inhibition/deletion accelerated thrombogenesis and elevated blood pressure in mice.
  • These adverse effects were attenuated by COX-1 knockdown.
  • mPGES-1 deletion reduced PGE(2) but increased PGI(2) expression without affecting thromboxane biosynthesis.
  • mPGES-1 deletion did not impact thrombogenesis or blood pressure.

Conclusions:

  • mPGES-1 inhibition may offer an alternative strategy for anti-inflammatory therapy.
  • Targeting mPGES-1 could suppress PGE(2) while avoiding the cardiovascular risks associated with PGHS-2 inhibition and PGI(2) suppression.