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001-es BibID:BIBFORM040823
035-os BibID:PMID:11238670
Első szerző:Sato, Koichiro
Cím:Carbon monoxide generated by heme oxygenase-1 suppresses the rejection of mouse-to-rat cardiac transplants / Koichiro Sato, Jozsef Balla, Leo Otterbein, R. Neal Smith, Sophie Brouard, Yuan Lin, Eva Csizmadia, Jean Sevigny, Simon C. Robson, Gregory Vercellotti, Augustine M. Choi, Fritz H. Bach, Miguel P. Soares
Dátum:2001
Megjegyzések:Mouse-to-rat cardiac transplants survive long term after transient complement depletion by cobra venom factor and T cell immunosuppression by cyclosporin A. Expression of heme oxygenase-1 (HO-1) by the graft vasculature is critical to achieve graft survival. In the present study, we asked whether this protective effect was attributable to the generation of one of the catabolic products of HO-1, carbon monoxide (CO). Our present data suggests that this is the case. Under the same immunosuppressive regimen that allows mouse-to-rat cardiac transplants to survive long term (i.e., cobra venom factor plus cyclosporin A), inhibition of HO-1 activity by tin protoporphyrin, caused graft rejection in 3--7 days. Rejection was associated with widespread platelet sequestration, thrombosis of coronary arterioles, myocardial infarction, and apoptosis of endothelial cells as well as cardiac myocytes. Under inhibition of HO-1 activity by tin protoporphyrin, exogenous CO suppressed graft rejection and restored long-term graft survival. This effect of CO was associated with inhibition of platelet aggregation, thrombosis, myocardial infarction, and apoptosis. We also found that expression of HO-1 by endothelial cells in vitro inhibits platelet aggregation and protects endothelial cells from apoptosis. Both these actions of HO-1 are mediated through the generation of CO. These data suggests that HO-1 suppresses the rejection of mouse-to-rat cardiac transplants through a mechanism that involves the generation of CO. Presumably CO suppresses graft rejection by inhibiting platelet aggregation that facilitates vascular thrombosis and myocardial infarction. Additional mechanisms by which CO overcomes graft rejection may involve its ability to suppress endothelial cell apoptosis.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:The Journal of Immunology 166 : 6 (2001), p. 4185-4194. -
További szerzők:Balla József (1959-) (belgyógyász, nephrológus) Otterbein, Leo Smith, R. Neal Brouard, Sophie Lin, Yuan Csizmadia Éva Sevigny, Jean Robson, Simon C. Vercellotti, Gregory M. Choi, Augustine Bach, Fritz H. Soares, Miguel P.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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