PURPOSE: The purpose of this study was to evaluate the expression of prostaglandin E2 (PGE2) and the two cyclooxygenase isoforms (cox1 and cox2) in human abdominal aortic aneurysm (AAA) tissue. METHODS: Ten specimens each of normal aortas and aneurysmal aortas were collected and used for histologic analysis and whole organ culture. An enzyme-linked immunosorbent assay for PGE2 was performed on the media from the aortic explant whole organ culture. An immunohistochemical analysis for PGE2 was performed, as was in situ hybridization for cox1 and cox2 on tissue sections. RESULTS: PGE2 production of AAA specimens was found to be 67,287 +/- 27,303 pg/ml as compared with 1698 +/- 858 pg/ml for normal aortic specimens (p < 0.001). PGE2 was localized by immunohistochemical analysis to the inflammatory infiltrate in AAAs. Minimal expression was noted in normal aortas. Using in situ hybridization, little expression of cox1 was noted in either the normal or the AAA specimens. Cox2 was expressed by macrophage-like cells within the inflammatory infiltrate of the AAA specimens but was not significantly expressed in the normal aorta. CONCLUSION: The expression of PGE2 is associated with the pathogenesis of human AAAs. Its expression is localized to macrophage-like cells within the inflammatory infiltrate and is controlled by the cox2 isoform of cyclooxygenase. Cox2 is, therefore, a potential target for pharmacotherapy of AAAs.
PURPOSE: The purpose of this study was to evaluate the expression of prostaglandin E2 (PGE2) and the two cyclooxygenase isoforms (cox1 and cox2) in humanabdominal aortic aneurysm (AAA) tissue. METHODS: Ten specimens each of normal aortas and aneurysmal aortas were collected and used for histologic analysis and whole organ culture. An enzyme-linked immunosorbent assay for PGE2 was performed on the media from the aortic explant whole organ culture. An immunohistochemical analysis for PGE2 was performed, as was in situ hybridization for cox1 and cox2 on tissue sections. RESULTS:PGE2 production of AAA specimens was found to be 67,287 +/- 27,303 pg/ml as compared with 1698 +/- 858 pg/ml for normal aortic specimens (p < 0.001). PGE2 was localized by immunohistochemical analysis to the inflammatory infiltrate in AAAs. Minimal expression was noted in normal aortas. Using in situ hybridization, little expression of cox1 was noted in either the normal or the AAA specimens. Cox2 was expressed by macrophage-like cells within the inflammatory infiltrate of the AAA specimens but was not significantly expressed in the normal aorta. CONCLUSION: The expression of PGE2 is associated with the pathogenesis of human AAAs. Its expression is localized to macrophage-like cells within the inflammatory infiltrate and is controlled by the cox2 isoform of cyclooxygenase. Cox2 is, therefore, a potential target for pharmacotherapy of AAAs.
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