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

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

Research output: Contribution to journalArticlepeer-review

19 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1-7
Number of pages7
JournalExperimental and Molecular Pathology
Volume93
Issue number1
DOIs
StatePublished - Aug 2012
Externally publishedYes

Keywords

  • Apoptosis
  • Cardiac fibroblast
  • IGF-1
  • Ischemia/reperfusion

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Molecular Biology
  • Clinical Biochemistry

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