Expression of NF-kappaB and Cytokines in Chronic Rejection of Transplanted Murine Heart
Journal of Korean Medical Science
;
: 397-406, 2001.
Artículo
en Inglés
| WPRIM
| ID: wpr-79896
ABSTRACT
The heart transplantation-associated accelerated graft arteriosclerosis (AGAS) is one of the major causes of cardiac allograft failure. We investigated the early time-course of expresssion patterns of cytokines, transcription factor, and its inhibitor in the intraabdominally transplanted mice hearts that differed only in the D locus of class I histocompatibility antigen. The allograft hearts were harvested at 1-3, 5, 7, 14, 28, and 42 days after the transplantation, and the expressions of NF-kappaB/I-kappaB and cytokines (TNF-alpha , INF-gamma) were examined in these specimens. The expressions of TNF-alpha and INF-gamma were observed on day 1, peaking on day 5 and 7, respectively. Activated NF-kappaB (p65) expression was present on the cytoplasm and perinuclear area in the endothelial cells of coronary arteries on day 1. The peak of translocation of NF-B from cytoplasm to nucleus appeared on day 5 in the endothelial cells, myocytes, and leukocytes within the vessels, and remained elevated until day 42. The I-kappaB expression gradually increased from day 1 until day 5, but a remarkable decrease was detected on day 7. Our data suggest that the increased expressions of NF-kappaB/I-kappaB and cytokines (TNF-alpha, INF-gamma) play an important role in inducing immune responses in the donor allograft heart and hence the blockage of the expressions might be mandatory to avoid a potential graft failure.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Trasplante Homólogo
/
Enfermedad de la Arteria Coronaria
/
Antígenos de Histocompatibilidad Clase I
/
Enfermedad Crónica
/
Citocinas
/
FN-kappa B
/
Trasplante de Corazón
/
Interferón gamma
/
Factor de Necrosis Tumoral alfa
/
Molécula 1 de Adhesión Intercelular
Límite:
Animales
Idioma:
Inglés
Revista:
Journal of Korean Medical Science
Año:
2001
Tipo del documento:
Artículo
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