JNK contributes to Hif-1α regulation in hypoxic neurons

Xanthi Antoniou, Alessandra Sclip, Cristina Ploia, Alessio Colombo, Gautier Moroy, Tiziana Borsello

Research output: Contribution to journalArticlepeer-review


Hypoxia is an established factor of neurodegeneration. Nowadays, attention is directed at understanding how alterations in the expression of stress-related signaling proteins contribute to age dependent neuronal vulnerability to injury. The purpose of this study was to investigate how Hif-1α, a major neuroprotective factor, and JNK signaling, a key pathway in neurodegeneration, relate to hypoxic injury in young (6DIV) and adult (12DIV) neurons. We could show that in young neurons as compared to mature ones, the protective factor Hif-1α is more induced while the stress protein phospho-JNK displays lower basal levels. Indeed, changes in the expression levels of these proteins correlated with increased vulnerability of adult neurons to hypoxic injury. Furthermore, we describe for the first time that treatment with the D-JNKI1, a JNK-inhibiting peptide, rescues adult hypoxic neurons from death and contributes to Hif-1α upregulation, probably via a direct interaction with the Hif-1α protein.

Original languageEnglish
Pages (from-to)114-127
Number of pages14
Issue number1
Publication statusPublished - Jan 2010


  • HIF-1α
  • Hypoxia
  • JNK
  • Neurons

ASJC Scopus subject areas

  • Organic Chemistry


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