期刊
TRANSPLANTATION
卷 87, 期 11, 页码 1645-1653出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/TP.0b013e3181a5c84c
关键词
Inflammation; Transplantation; Macrophages; Transcriptional factors
资金
- Japanese Ministry of Education, Science and Culture
- Japanese Ministry of Welfare
- US National Heart Lung and Blood Institute [HL34636]
- Foundation Leducq to Dr. Peter Libby
- Women's Hospital and the Harvard Medical School
Background. Prostaglandin E-2 (PGE(2)) is a pathogenesis of inflammatory diseases; PGE(2) plays a key role in association of anti-inflammation and immune suppression. EP4, which is a PGE(2) receptor, is known to suppress the production of inflammatory cytokines and chemokines in vitro. Although it has been reported that EP4 agonists prolonged cardiac allograft survival, little has been elucidated the immunologic mechanism. Methods. We injected a selective EP4 agonist (EP4RAG) into recipient mice with heterotopic cardiac transplantation. Results. EP4RAG significantly prolonged the graft survival compared with the vehicle-treated group. Although the vehicle-treated group showed severe myocardial cell infiltration, the EP4RAG-treated group attenuated the development on day 7. EP4RAG suppressed various proinflammatory factors such as cytokines, chemokines, adhesion molecules, and nuclear factor-kappa B (NF-kappa B) compared with the vehicle-treated group. We also demonstrated that EP4RAG suppressed the activation of macrophages, but it did not affect to T lymphocytes in vitro. EP4RAG inhibited the activation of NF-kappa B compared with the control group. Conclusion. Pharmacological selective EP4 activation suppressed the production of proinflammatory factors by inhibition of NF-kappa B activity in cardiac transplantation.
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