Cardiotrophin-1 protects cortical neuronal cells against free radical-induced injuries in vitro

Tong Chun Wen, Marta R. Rogido, James E. Moore, Tom Genetta, Hui Peng, Augusto Sola

Research output: Contribution to journalArticlepeer-review

24 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)38-42
Number of pages5
JournalNeuroscience letters
Issue number1
StatePublished - Oct 14 2005


  • Cardiotrophin-1
  • Free radicals
  • Neuron culture
  • Neuroprotection

ASJC Scopus subject areas

  • Neuroscience(all)


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