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Consequences of altered eicosanoid patterns for nociceptive processing in mPGES-1-deficient mice
Christian Brenneis1, Ovidiu Coste, Ronald Schmidt
1Pharmazentrum Frankfurt, ZAFES, Institut für Klinische Pharmakologie, Klinikum der Johann Wolfgang Goethe-Universität Theodor-Stern-Kai 7, Frankfurt, Germany.
Journal of Cellular and Molecular Medicine
|April 19, 2008
Summary
Microsomal prostaglandin E2 synthase-1 (mPGES-1) deficiency surprisingly did not reduce pain behaviors in mice. This suggests other prostaglandins may compensate for the loss of PGE2 in pain signaling.
Area of Science:
- Neuroscience
- Immunology
- Biochemistry
Background:
- Spinal cord cyclooxygenase-2 (COX-2)-dependent prostaglandin E2 (PGE2) synthesis is crucial for inflammatory pain (hyperalgesia and allodynia).
- Microsomal PGE2 synthase-1 (mPGES-1) converts COX-2-derived prostaglandin H2 (PGH2) into PGE2.
Purpose of the Study:
- To investigate the role of mPGES-1 in nociceptive behavior in models dependent on PGE2 synthesis.
- To determine if mPGES-1 deficiency impacts pain perception.
Main Methods:
- Evaluation of nociceptive behavior in mPGES-1-deficient mice using zymosan-evoked hyperalgesia and formalin tests.
- Analysis of prostaglandin synthesis in spinal cords and primary spinal cord cells from mPGES-1-deficient mice.
Main Results:
- Mice lacking mPGES-1 showed no reduction in nociceptive behavior in the zymosan-evoked hyperalgesia model, despite decreased spinal PGE2.
- Nociceptive behavior remained unaltered in mPGES-1-deficient mice during the formalin test.
- Spinal cells from mPGES-1-deficient mice exhibited a shift in synthesis from PGE2 to prostaglandin D2 (PGD2), prostaglandin F2alpha (PGF2alpha), and 6-keto-PGF1alpha (a PGI2 metabolite).
Conclusions:
- The absence of mPGES-1 does not attenuate inflammatory pain behaviors.
- Compensatory synthesis of other prostaglandins (PGD2, PGF2alpha, PGI2) may play a role in nociception, potentially explaining the unaltered pain response in mPGES-1-deficient mice.
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