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Apollon/Bruce is upregulated by Humanin.

Yuichi Hashimoto1, Yuji Takeshita, Mikihiko Naito

  • 1Department of Pharmacology, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, Tokyo, 160-8402, Japan.

Molecular and Cellular Biochemistry
|August 21, 2014
PubMed
Summary

Humanin peptide protects against Alzheimer's disease (AD) linked neuronal death by upregulating Apollon/Bruce, an inhibitor of apoptosis protein. This pathway involves the heterotrimeric Humanin receptor (htHNR), JAKs, and STAT3 signaling.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Humanin is a bioactive peptide that prevents various cell deaths, including neuronal cell death linked to Alzheimer's disease (AD).
  • Humanin's protective effect involves binding to its receptor (htHNR), activating the JAKs/STAT3 pathway, and upregulating SH3BP5, an effector of anti-cell death activity.

Purpose of the Study:

  • To investigate if SH3BP5 is the sole effector of the Humanin signaling pathway via htHNR/JAKs/STAT3.
  • To identify other potential effectors in the Humanin-mediated neuroprotective signaling cascade.

Main Methods:

  • Utilized cell culture models expressing AD-linked mutant amyloid precursor protein (APP V642I).
  • Analyzed the Humanin signaling pathway (htHNR/JAKs/STAT3) activation.
  • Measured mRNA and protein expression levels of Apollon/Bruce.
  • Assessed the effect of Apollon/Bruce overexpression on neuronal cell death.

Main Results:

  • The Humanin/htHNR/JAKs/STAT3 pathway significantly increased both mRNA and protein levels of Apollon/Bruce.
  • Overexpression of Apollon/Bruce demonstrated a protective effect against neuronal death induced by the AD-linked APP V642I mutation.
  • Apollon/Bruce was identified as a novel effector of Humanin's anti-apoptotic activity.

Conclusions:

  • Humanin upregulates the expression of Apollon/Bruce through the htHNR/JAKs/STAT3 pathway.
  • Apollon/Bruce acts as a context-dependent effector of Humanin's neuroprotective function in Alzheimer's disease models.
  • These findings expand the understanding of Humanin's mechanism of action in preventing neuronal cell death.