Serum Prostaglandin D Synthase Level after Coronary Angioplasty May Predict Occurrence of Restenosis

Teruo Inoue; Kan Takayanagi; Shigenori Morooka; Yoshio Uehara; Hiroshi Oda; Kousuke Seiki; Hiroshi Nakajima; Yoshihiro Urade

doi:10.1055/s-0037-1612920

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 2001; 85(01): 165-170
DOI: 10.1055/s-0037-1612920

Review Article

Schattauer GmbH

Serum Prostaglandin D Synthase Level after Coronary Angioplasty May Predict Occurrence of Restenosis

Teruo Inoue

¹Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine Koshigaya, Suita, Japan

,

Kan Takayanagi

¹Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine Koshigaya, Suita, Japan

,

Shigenori Morooka

²Health Service Center, University of Tokyo, Tokyo, Japan

,

Yoshio Uehara

²Health Service Center, University of Tokyo, Tokyo, Japan

,

Hiroshi Oda

³Central Research Institute, Maruha Corporation, Tsukuba, Japan

,

Kousuke Seiki

³Central Research Institute, Maruha Corporation, Tsukuba, Japan

,

Hiroshi Nakajima

³Central Research Institute, Maruha Corporation, Tsukuba, Japan

,

Yoshihiro Urade

⁴Core Research for Evolutional Science and Technology, Japan, Science and Technology Corporation, c/o Department of Molecular and Behavioral Biology, Osaka Bioscience Institute, Suita, Japan

› Author Affiliations

Abstract

Summary

Lipocalin-type prostaglandin D synthase (L-PGDS), which is responsible for the biosynthesis of PGD₂, has recently been found to be present in the atherosclerotic plaque of the human coronary artery and also to be secreted in human serum. We measured the serum L-PGDS level and compared it with the expressions of the platelet membrane surface glycoprotein and neutrophil adhesion molecule in patients undergoing PTCA. The L-PGDS level significantly decreased (P < 0.01) and the platelet surface expression of CD62P (P-selectin) significantly increased (P < 0.01) immediately after PTCA in the coronary sinus blood. Both changes were inversely correlated (R = −0.72, P < 0.001). Although the L-PGDS level in the coronary sinus blood remained equivalent to the baseline level in patients who experienced restenosis, the level increased over the baseline level (P < 0.01) at 48 h after PTCA in patients without restenosis. Neutrophil surface expression of CD11b (a subunit of Mac-1) significantly increased at 24 h (P < 0.01) to 48 h (P < 0.001) after PTCA in the coronary sinus blood in patients with restenosis but the change showed less significant in patients without restenosis. The changes in the L-PGDS level and the CD11b expression at 48 h after PTCA were inversely correlated (R = −0.55, P < 0.05). An increased serum L-PGDS level at 48 h after PTCA possibly predicts the avoidance of late restenosis. It is suggested that reduction in PGD₂ synthesis triggers platelet activation and that a subsequent increase in the PGD₂ synthesis suppresses inflammatory reaction at the intervention site indicated by neutrophil activation and inhibits development of restenosis. Pharmacological or biological intervention that increases endogenous PGD₂ synthesis should be tested as a new strategy to prevent restenosis.

Keywords

Prostaglandin D synthase - prostaglandin D₂ - platelet - neutrophil - restenosis

Full Text

References

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