Prolonged activation of transcription factor AP-1 during NGF-mediated rescue from apoptotic cell death in PC12 cells

Liqi Tong, Karin Werrbach-Perez, J. Regino Perez-Polo

    Research output: Contribution to journalArticlepeer-review

    13 Scopus citations

    Abstract

    Rat pheochromocytoma (PC12) cells exhibit apoptotic cell death when deprived of serum and can be rescued by nerve growth factor (NGF). We characterized AP-1 DNA binding activity in PC12 cells after serum deprivation in the presence or absence of NGF or other neurotrophic agents. There was a decline in AP-1 DNA binding activity concomitant with apoptosis in PC12 cells after serum deprivation. Treatment of serum-deprived PC12 with NGF induced persistent AP-1 binding activity that was blocked by the Trk receptor inhibitor K252a. PC12 cells treated with dibutyryl cyclic AMP or insulin also displayed increased AP-1 DNA binding activity. While NGF somewhat increased c-Fos and c-Jun protein levels transiently, it had a more robust and persistent stimulatory effect on Jun B protein levels. AP-1 transcriptional activity increased after NGF, dibutyryl cAMP, or insulin treatment under serum free conditions. Curcumin, which inhibits AP-1 activity, blocked the NGF-mediated rescue. These results would suggest that the rescue of serum- deprived PC12 cells from apoptosis requires increasing endogenous levels of specific Fos/Jun components of AP-1.

    Original languageEnglish (US)
    Pages (from-to)1431-1441
    Number of pages11
    JournalNeurochemical Research
    Volume24
    Issue number11
    DOIs
    StatePublished - 1999

    Keywords

    • AP-1
    • Apoptotic cell death
    • NGF
    • PCI2
    • Serum deprivation

    ASJC Scopus subject areas

    • Biochemistry
    • Cellular and Molecular Neuroscience

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