Thromb Haemost 2004; 92(05): 925-928
DOI: 10.1160/TH04-05-0302
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Cyclooxygenase COX-2a, a novel COX-2 mRNA variant, in platelets from patients after coronary artery bypass grafting

Petra Censarek
1   Institut für Pharmakologie and Klinische Pharmakologie, Universitätsklinikum Düsseldorf, Düsseldorf, Germany
,
Kerstin Freidel
1   Institut für Pharmakologie and Klinische Pharmakologie, Universitätsklinikum Düsseldorf, Düsseldorf, Germany
,
Michael Udelhoven
1   Institut für Pharmakologie and Klinische Pharmakologie, Universitätsklinikum Düsseldorf, Düsseldorf, Germany
,
Sun-Jung Ku
1   Institut für Pharmakologie and Klinische Pharmakologie, Universitätsklinikum Düsseldorf, Düsseldorf, Germany
,
Thomas Hohlfeld
1   Institut für Pharmakologie and Klinische Pharmakologie, Universitätsklinikum Düsseldorf, Düsseldorf, Germany
,
Jutta Meyer-Kirchrath
1   Institut für Pharmakologie and Klinische Pharmakologie, Universitätsklinikum Düsseldorf, Düsseldorf, Germany
,
Karsten Schrör
1   Institut für Pharmakologie and Klinische Pharmakologie, Universitätsklinikum Düsseldorf, Düsseldorf, Germany
,
Artur-Aron Weber
1   Institut für Pharmakologie and Klinische Pharmakologie, Universitätsklinikum Düsseldorf, Düsseldorf, Germany
› Author Affiliations
Financial support: This work was supported by the Deutsche Forschungsgemeinschaft (WE-2355/2-1).
Further Information

Publication History

Received 14 May 2004

Accepted after revision 13 August 2004

Publication Date:
04 December 2017 (online)

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Summary

There are two principal cyclooxygenase isoforms referred to as COX-1 and COX-2. Recently, COX-3 has been identified. We have demonstrated the expression of COX-2 in platelets from patients after coronary artery bypass grafting (CABG). Careful biochemical analysis revealed that, when compared to recombinant COX-2, platelet COX-2 had a slightly higher electrophoretic mobility. Two COX-2 sequences (∼1.8 kb, ∼1.7 kb) were cloned from platelet mRNA. The ∼1.7 kb sequence, designated COX-2a, differed from the human COX-2 sequence only in a deletion from position +458 to +567. Similar to the human COX-3, there is a frame shift in the COX-2a sequence resulting in a TAA stop codon at position +490. Thus, the expression of a COX-2a protein corresponding to the 67 kDa COX-2 protein is not clear. However, the marked shifting from COX-2 to COX-2a in platelets from some patients after CABG is a striking finding.