title: Cardiotrophin-1 protects cortical neuronal cells against free radical-induced injuries in vitro.
abstract: Cardiotrophin-1 (CT-1) was initially defined as a mediator of cardiomyocyte hypertrophy. Additional studies have showed that CT-1 enhanced survival of differentiated cardiac muscle cells and inhibited cardiac myocyte apoptosis after serum deprivation or cytokine stimulation. Moreover, CT-1 has recently been shown to act as a neuroregulatory cytokine in the peripheral nervous system. However, its effects in the central nervous system have not been determined. In the present study, we evaluated whether CT-1 protects cultured cortical neurons against oxidative injuries caused by the hydroxyl radical-producing agent FeSO4 and by the peroxynitrite-producing agent 3-morpholinosydnonimine (SIN-1). CT-1 reduced neuronal cell death caused by FeSO4 and also attenuated the neurotoxic effect of SIN-1 in a dose-dependent manner. These results indicate that CT-1 is neuroprotective in an in vitro model of cerebral ischemia. This study indicates that further evaluation of CT-1 in acute brain injury should be investigated in vivo.
authors.affiliation: Division of Neonatal-Perinatal Medicine, Department of Pediatrics, Emory University School of Medicine, 2015 Uppergate Drive, Atlanta, GA 30322, USA. Tong_wen@oz.ped.emory.edu
authors.forename: Tong-Chun
authors.initials: TC
authors.lastname: Wen
authors.forename: Marta R
authors.initials: MR
authors.lastname: Rogido
authors.forename: James E
authors.initials: JE
authors.lastname: Moore
authors.forename: Tom
authors.initials: T
authors.lastname: Genetta
authors.forename: Hui
authors.initials: H
authors.lastname: Peng
authors.forename: Augusto
authors.initials: A
authors.lastname: Sola
mesh_terms: D000818:Animals; D001925:Brain Damage, Chronic / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control; D002545:Brain Ischemia / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D002544:Cerebral Infarction / Q000188:drug therapy / Q000503:physiopathology / Q000517:prevention & control; D016207:Cytokines / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005290:Ferric Compounds / Q000009:adverse effects / Q000037:antagonists & inhibitors; D016166:Free Radical Scavengers / Q000494:pharmacology; D005609:Free Radicals / Q000009:adverse effects / Q000037:antagonists & inhibitors*; D008981:Molsidomine / Q000009:adverse effects / Q000031:analogs & derivatives / Q000037:antagonists & inhibitors; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D051381:Rats
chemical_list: D016207:Cytokines; D005290:Ferric Compounds; D016166:Free Radical Scavengers; D005609:Free Radicals; D018696:Neuroprotective Agents; C024823:ferric sulfate; C002385:linsidomine; C092073:cardiotrophin 1; D008981:Molsidomine