Homocysteine-induced toxicity increases TG2 expression in Neuro2a cells

M. Currò, S. Condello, D. Caccamo, N. Ferlazzo, G. Parisi, R. Ientile*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


High levels of homocysteine promote cell damage mainly through induction of oxidative stress, endoplasmic reticulum (ER) stress, and activation of pro-inflammatory factors. The effects of homocysteine were here examined in the continuously dividing neuroblastoma cell line Neuro2a. Cell treatment with homocysteine (100-500 μM) for 4 h increased ROS production while reducing cell viability in a dose-dependent manner. Cell exposure to 250 μM homocysteine was able to induce transglutaminase 2 up-regulation and increased in situ transglutaminase activity. These effects were prevented by the incubation with the transglutaminase activity inhibitor cystamine. Homocysteine also induced NF-κB activation that seemed associated with transglutaminase 2 up-regulation since the specific NF-κB inhibition by SN50 was able to reduce transglutaminase expression and activity levels. In the light of these observations, it may be postulated that TG2 up-regulation is involved in cell response to homocysteine-induced stress, in which NF-κB activation plays also a pivotal role.

Original languageEnglish (US)
Pages (from-to)725-730
Number of pages6
JournalAmino Acids
Issue number4
StatePublished - Apr 1 2009


  • Homocysteine
  • NF-κB
  • Neuro2a cells
  • ROS
  • Transglutaminases

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry
  • Organic Chemistry


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