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

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• 作者：Raú ; l Vivar¹ ; Claudio Humeres¹ ; Marcelo Varela ; Pedro Ayala ; Nancy Guzmá ; n ; Ivonne Olmedo ; Mabel Catalá ; n ; Pí ; a Boza ; Claudia Muñ ; oz ; Guillermo Dí ; az Araya ; ^{gadiaz@ciq.uchile.cl}
• 关键词：CF ; cardiac fibroblast ; I/R ; ischemia/reperfusion ; FBS ; fetal bovine serum ; FCS ; fetal calf serum ; ECL ; enhanced chemiluminescence ; PI ; propidium iodide
• 刊名：Experimental and Molecular Pathology
• 出版年：2012
• 期刊代码：291_00144800
• 类别：med
• 出版时间：August, 2012
• 卷：93
• 期：1
• 页码：1-7
• 文件大小：613 K

摘要

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.