EXPRESSION OF LIPOCALIN-TYPE PROSTAGLANDIN-D SYNTHASE (BETA-TRACE) INHUMAN HEART AND ITS ACCUMULATION IN THE CORONARY CIRCULATION OF ANGINA PATIENTS

Citation
Y. Eguchi et al., EXPRESSION OF LIPOCALIN-TYPE PROSTAGLANDIN-D SYNTHASE (BETA-TRACE) INHUMAN HEART AND ITS ACCUMULATION IN THE CORONARY CIRCULATION OF ANGINA PATIENTS, Proceedings of the National Academy of Sciences of the United Statesof America, 94(26), 1997, pp. 14689-14694
Citations number
38
ISSN journal
00278424
Volume
94
Issue
26
Year of publication
1997
Pages
14689 - 14694
Database
ISI
SICI code
0027-8424(1997)94:26<14689:EOLPS(>2.0.ZU;2-D
Abstract
Lipocalin-type prostaglandin D synthase (L-PGDS) is localized in the c entral nervous system and male genital organs of various mammals and i s secreted as p-trace into the closed compartment of these tissues sep arated from the systemic circulation. In this study, we found that the mRNA for the human enzyme was expressed most intensely in the heart a mong various tissues examined. In human autopsy specimens, the enzyme was localized immunocytochemically in myocardial cells, atrial endocar dial cells, and a synthetic phenotype of smooth muscle cells in the ar teriosclerotic intima, and accumulated in the atherosclerotic plaque o f coronary arteries with severe stenosis. In patients with stable angi na (75-99% stenosis), the plasma level of L-PGDS was significantly (P < 0.05) higher in the great cardiac vein (0.694 +/- 0.054 mu g/ml, n = 7) than in the coronary artery (0.545 +/- 0.034 mu g/ml), as determin ed by a sandwich enzyme immunoassay. However, the veno-arterial differ ence in the plasma L-PGDS concentration was not observed in normal sub jects without stenosis. After a percutaneous transluminal coronary ang ioplasty was performed to compress the stenotic atherosclerotic plaque s, the L-PGDS concentration in the cardiac vein decreased significantl y (P < 0.05) to 0.610 +/- 0.051 mu g/ml at 20 min and reached the arte rial level within 1 h. These findings suggest that L-PGDS is present i n both endocardium and myocardium of normal subjects and the stenotic site of patients with stable angina and is secreted into the coronary circulation.