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Cardiac fibroblast death by ischemia/reperfusion is partially inhibited by IGF-1 through both PI3K/Akt and MEK–ERK pathways

2012; Elsevier BV; Volume: 93; Issue: 1 Linguagem: Inglês

10.1016/j.yexmp.2012.01.010

1096-0945

Raúl Vivar, Claudio Humeres, Marcelo Varela, Pedro Ayala, Nancy Guzmán, Ivonne Olmedo, Mabel Catalán, Pía Boza, Claudia Muñoz, Guillermo Díaz Araya,

Cardiac electrophysiology and arrhythmias

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.IGF-1 partially inhibits CF apoptosis induced by simulated I/R by PI3K/Akt- and MEK/ERK1/2-dependent signaling pathways.