title: Soluble TRAIL prevents RANTES-dependent restenosis after percutaneous coronary intervention in patients with coronary artery disease.
abstract: Some factors play pathogenic roles in the development of restenosis after percutaneous coronary intervention (PCI). We measured and compared the ratio of elevated levels of regulated on activation normally T-cell expressed and secreted (RANTES), soluble (s) P-selectin, sE-selectin, s vascular cell adhesion molecule (VCAM)-1, s interleukin-2 receptor (IL-2R) and s tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) after PCI. Plasma levels of chemokines and soluble markers were measured before and 30 days after PCI in 85 patients (61 males and 24 females, aged 61 +/- 7 years) who underwent PCI and who had repeated angiograms at a 6-month follow-up. Restenosis occurred in 29 (34.1%) patients. The significant and time-dependent increases in RANTES, sIL-2R and sVCAM-1 were observed in the restenosis group. However, there were no significant differences in sP-selectin and sE-selectin levels with or without restenosis. sTRAIL levels in patients with coronary artery disease were significantly higher than levels in normal controls. Furthermore, unlike the restenosis group, sTRAIL levels after PCI were significantly increased in the non-restenosis group, and sTRAIL levels correlated significantly with sVCAM-1 and sE-selectin. These findings suggest that restenosis development after PCI in patients with coronary artery disease involve the participation of RANTES and activated T-lymphocyte expressing CD25 after PCI, and sTRAIL may prevent this RANTES-dependent restenosis.
authors.affiliation: Second Department of Internal Medicine, Kansai Medical University, Moriguchi, Osaka, Japan.
authors.forename: Daisuke
authors.initials: D
authors.lastname: Satoh
authors.forename: Norihito
authors.initials: N
authors.lastname: Inami
authors.forename: Takayuki
authors.initials: T
authors.lastname: Shimazu
authors.forename: Takayuki
authors.initials: T
authors.lastname: Kajiura
authors.forename: Kohichi
authors.initials: K
authors.lastname: Yamada
authors.forename: Toshiji
authors.initials: T
authors.lastname: Iwasaka
authors.forename: Shosaku
authors.initials: S
authors.lastname: Nomura
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D015415:Biomarkers / Q000097:blood; D018946:Chemokine CCL5 / Q000097:blood*; D003324:Coronary Artery Disease / Q000097:blood* / Q000628:therapy; D023903:Coronary Restenosis / Q000097:blood* / Q000188:drug therapy / Q000209:etiology / Q000517:prevention & control; D019040:E-Selectin / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D053645:Interleukin-2 Receptor alpha Subunit / Q000097:blood; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000097:blood; D013601:T-Lymphocytes / Q000378:metabolism; D053221:TNF-Related Apoptosis-Inducing Ligand / Q000097:blood* / Q000627:therapeutic use; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D015415:Biomarkers; C483024:CCL5 protein, human; D018946:Chemokine CCL5; D019040:E-Selectin; C508017:IL2RA protein, human; D053645:Interleukin-2 Receptor alpha Subunit; D019007:P-Selectin; D053221:TNF-Related Apoptosis-Inducing Ligand; C505653:TNFSF10 protein, human; D019010:Vascular Cell Adhesion Molecule-1