title: Cardiac fibroblast death by ischemia/reperfusion is partially inhibited by IGF-1 through both PI3K/Akt and MEK-ERK pathways.
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.
  
  
  CONCLUSIONS
  IGF-1 partially inhibits CF apoptosis induced by simulated I/R by PI3K/Akt- and MEK/ERK1/2-dependent signaling pathways.
authors.affiliation: Laboratorio de Farmacoquímica y Centro FONDAP CEMC, Centro de Estudios Moleculares de Célula, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile.
authors.forename: Raúl
authors.initials: R
authors.lastname: Vivar
authors.forename: Claudio
authors.initials: C
authors.lastname: Humeres
authors.forename: Marcelo
authors.initials: M
authors.lastname: Varela
authors.forename: Pedro
authors.initials: P
authors.lastname: Ayala
authors.forename: Nancy
authors.initials: N
authors.lastname: Guzmán
authors.forename: Ivonne
authors.initials: I
authors.lastname: Olmedo
authors.forename: Mabel
authors.initials: M
authors.lastname: Catalán
authors.forename: Pía
authors.initials: P
authors.lastname: Boza
authors.forename: Claudia
authors.initials: C
authors.lastname: Muñoz
authors.forename: Guillermo
authors.initials: G
authors.lastname: Díaz Araya
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis / Q000187:drug effects*; D002478:Cells, Cultured; D002867:Chromones / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005347:Fibroblasts / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D005419:Flavonoids / Q000494:pharmacology; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology*; D020935:MAP Kinase Signaling System / Q000187:drug effects / Q000502:physiology*; D009025:Morpholines / Q000494:pharmacology; D000081082:Phosphoinositide-3 Kinase Inhibitors; D051057:Proto-Oncogene Proteins c-akt / Q000037:antagonists & inhibitors; D051381:Rats; D015427:Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D002867:Chromones; D004791:Enzyme Inhibitors; D005419:Flavonoids; D009025:Morpholines; D000081082:Phosphoinositide-3 Kinase Inhibitors; C085911:2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; D007334:Insulin-Like Growth Factor I; D051057:Proto-Oncogene Proteins c-akt; C093973:2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one