Clinical Chemistry and Laboratory Medicine (CCLM)
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The c.–292C>T promoter polymorphism increases reticulocyte-type 15-lipoxygenase-1 activity and could be atheroprotective
- 1Institute of Clinical Chemistry, Center for Integrative Human Physiology, University Hospital Zurich, Zurich, Switzerland
- 2Department of Food Chemistry, J.W. Goethe-University, Biocenter, Frankfurt am Main, Germany
- 3Department of Food Chemistry, J.W. Goethe-University, Biocenter, Frankfurt am Main, Germany
- 4Cardiovascular Center Division of Cardiology, University Hospital Zurich, Zurich, Switzerland
- 5Institute of Clinical Chemistry, Center for Integrative Human Physiology, University Hospital Zurich, Zurich, Switzerland
Background: Reticulocyte-type 15-lipoxygenase-1 (ALOX15) has anti-inflammatory and inflammatory effects and is implicated in the development of asthma, arthritis and atherosclerosis. Previously, we screened the human ALOX15 gene for variations because genetic variability in ALOX15 might influence these diseases. We found a C>T substitution at position c.–292 in the ALOX15 promoter that created a novel binding site for the transcription factor SPI1 and increased ALOX15 mRNA levels in monocytes from c.–292CT heterozygous volunteers.
Methods: To test whether the higher mRNA levels led to higher ALOX15 activity, we performed an activity assay and measured the arachidonic acid metabolite 15(S)-hydroxy-eicosatetraenoic acid [15(S)-HETE] by HPLC analysis. To test whether this polymorphism was associated with coronary artery disease (CAD), we investigated its association in a case-control study involving 498 Caucasians.
Results: The c.–292C>T polymorphism was associated with higher enzyme activity in heterozygous carriers. Intriguingly, this polymorphism also showed a tendency to be protective against atherosclerosis.
Conclusions: These results suggest that increased ALOX15 activity may attenuate inflammation, which could be caused by an increase in 15(S)-HETE and eventually by its metabolites, the lipoxins.
Clin Chem Lab Med 2007;45:487–92.
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