Soluble TRAIL prevents RANTES-dependent restenosis after percutaneous coronary intervention in patients with coronary artery disease View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2010-05

AUTHORS

Daisuke Satoh, Norihito Inami, Takayuki Shimazu, Takayuki Kajiura, Kohichi Yamada, Toshiji Iwasaka, Shosaku Nomura

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. More... »

PAGES

471-476

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s11239-009-0364-9

DOI

http://dx.doi.org/10.1007/s11239-009-0364-9

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1024086051

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/19533303


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