title: Antithrombotic effects of endocardial endothelial cells-comparison with coronary artery endothelial cells.
abstract: The purpose of this study was to assess the anti-platelet properties of endocardial endothelial cells (EECs) by measuring platelet aggregation after a brief incubation with cultured EECs. EECs were isolated from the right ventricles of porcine hearts and coronary artery endothelial cells (C-ECs) were also isolated from the same animals. After brief incubations (2-min) of platelet suspensions with cultured EEC and CEC monolayers, platelet aggregation in response to thrombin and 6-keto-PGF1 alpha (a stable metabolite of PGI2) content of platelet suspensions were measured. Platelet aggregation was significantly inhibited by a brief incubation of platelet suspensions with EEC and C-ECs monolayers. Pretreatment of EECs and C-ECs with indomethacin (5 x 10(-5) M) restored platelet activity, but pretreatment with N omega-nitro-L-arginine methyl ester (L-NAME, 5 x 10(-5) M) or hemoglobin (1 x 10(-6) M) did not. Platelet/EEC interactions multiplicatively increased the 6-keto-PGF1 alpha content of platelet suspensions and the 6-keto-PGF1 alpha content of platelet suspensions after incubations with EECs correlated significantly with the inhibition of platelet aggregation. Both the anti-aggregation properties and 6-keto-PGF1 alpha production were significantly greater in EECs than in C-ECs. A brief incubation (2-min) with PDGF (10 ng/ml) or TGF-beta (1 and 10 ng/ml) stimulated 6-keto-PGF1 alpha production in EECs but not in C-ECs, although these growth factors stimulated 6-keto-PGF1 alpha production in C-ECs after a longer incubation time (30 or 60 min). In this study, after a brief incubation (2-min) with platelet suspensions, EECs inhibited platelet aggregation mainly through the release of PGI2 but not EDRF. As this anti-aggregation property was significantly greater in EECs than in C-ECs, it is suggested that endocardial endothelial PGI2 may inhibit both intracardiac and intracoronary artery thrombus formation, contributing to the prevention of myocardial ischemia.
authors.affiliation: First Department of Surgery, Shimane Medical University, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Nosaka
authors.forename: M
authors.initials: M
authors.lastname: Hashimoto
authors.forename: T
authors.initials: T
authors.lastname: Sasaki
authors.forename: K
authors.initials: K
authors.lastname: Ku
authors.forename: Y
authors.initials: Y
authors.lastname: Saitoh
authors.forename: T
authors.initials: T
authors.lastname: Hanada
authors.forename: M
authors.initials: M
authors.lastname: Yamauchi
authors.forename: S
authors.initials: S
authors.lastname: Masumura
authors.forename: K
authors.initials: K
authors.lastname: Nakayama
authors.forename: K
authors.initials: K
authors.lastname: Tamura
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism*; D000818:Animals; D001792:Blood Platelets / Q000502:physiology*; D002452:Cell Count; D002478:Cells, Cultured; D004699:Endocardium / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D004727:Endothelium / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D011464:Epoprostenol / Q000378:metabolism*; D007213:Indomethacin / Q000494:pharmacology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D010974:Platelet Aggregation; D010982:Platelet-Derived Growth Factor / Q000494:pharmacology; D013552:Swine; D013917:Thrombin / Q000494:pharmacology; D016212:Transforming Growth Factor beta / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D010982:Platelet-Derived Growth Factor; D016212:Transforming Growth Factor beta; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol; D013917:Thrombin; D019331:NG-Nitroarginine Methyl Ester; D007213:Indomethacin