Cardiac fibroblast death by ischemia/reperfusion is partially inhibited by IGF-1 through both PI3K/Akt and MEK-ERK pathways.
Exp Mol Pathol
; 93(1): 1-7, 2012 Aug.
Article
en En
| MEDLINE
| ID: mdl-22537549
ABSTRACT
UNLABELLED Cardiac fibroblast (CF) death by ischemia/reperfusion (I/R) has major implications for cardiac wound healing. Although IGF-1 has well-known cytoprotective effects, no study has been done on CF subjected to simulated I/R. Simulated ischemia of neonate rat CF was performed in a free oxygen chamber in an ischemic medium; reperfusion was done in normal culture conditions. Cell viability was evaluated by trypan blue assay, and apoptosis by a FACS flow cytometer; p-ERK-1/2 and p-Akt levels were determined by western blot. We showed that simulated I/R triggers CF death by necrosis and apoptosis. IGF-1 partially inhibits I/R-induced apoptosis. PD98059 and LY294002 neutralize the preventive effects of IGF-1. CONCLUSION:
IGF-1 partially inhibits CF apoptosis induced by simulated I/R by PI3K/Akt- and MEK/ERK1/2-dependent signaling pathways.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Factor I del Crecimiento Similar a la Insulina
/
Daño por Reperfusión
/
Apoptosis
/
Sistema de Señalización de MAP Quinasas
/
Fibroblastos
Límite:
Animals
Idioma:
En
Revista:
Exp Mol Pathol
Año:
2012
Tipo del documento:
Article
País de afiliación:
Chile