A femtomolar-acting neuroprotective peptide induces increased levels of heat shock protein 60 in rat cortical neurons: A potential neuroprotective mechanism

Rachel Zamostiano, Albert Pinhasov, Merav Bassan, Orly Perl, Ruth A. Steingart, Roy Atlas, Douglas E. Brenneman, Illana Gozes*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Activity-dependent neurotrophic factor (ADNF) was recently isolated from conditioned media of astrocytes stimulated with vasoactive intestinal peptide (VIP). ADNF provided neuroprotection at femtomolar concentration against a wide variety of toxic insults. A nine amino acid peptide (ADNF-9) captured with even greater potency the neuroprotective activity exhibited by the parent protein. Utilizing Northern and Western blot analyses, it was now shown that ADNF-9 increased the expression of heat shock protein 60 (hsp60) in rat cerebral cortical cultures. In contrast, treatment with the Alzheimer's toxin, the β-amyloid peptide, reduced the amount of intracellular hsp60. Treatment with ADNF-9 prevented the reduction in hsp60 produced by the β-amyloid peptide. The protection against the β-amyloid peptide-associated cell death provided by ADNF-9 may be mediated in part by intracellular increases in hsp60.

Original languageEnglish
Pages (from-to)9-12
Number of pages4
JournalNeuroscience Letters
Volume264
Issue number1-3
DOIs
StatePublished - 2 Apr 1999

Funding

FundersFunder number
United States-Israel Binational Science Foundation

    Keywords

    • Activity-dependent neurotrophic factor
    • Neurons
    • Stress proteins
    • hsp60

    Fingerprint

    Dive into the research topics of 'A femtomolar-acting neuroprotective peptide induces increased levels of heat shock protein 60 in rat cortical neurons: A potential neuroprotective mechanism'. Together they form a unique fingerprint.

    Cite this