IL-5 blocks apoptosis and tau hyperphosphorylation induced by Aβ 25-35 peptide in PC12 cells

J Physiol Biochem. 2017 May;73(2):259-266. doi: 10.1007/s13105-017-0550-8. Epub 2017 Jan 28.

Abstract

The primary features of Alzheimer's disease (AD) are extracellular amyloid plaques consisting mainly of deposits of amyloid β (Aβ) peptides and intracellular neurofibrillary tangles (NFTs). Sets of evidence suggest that interleukin-5 (IL-5) is involved in the pathogenesis of AD. Herein, we investigated the protective role of IL-5 in PC12 cells, to provide new insights into understanding this disease. Western blot was employed to assess the protein levels of Bax and phospho-tau as well as phospho-JAK2; MTT assay was performed to decipher cell viability. Treatment of IL-5 decreased Aβ25-35-induced tau phosphorylation and apoptosis, effects blunted by JAK2 inhibition. IL-5 prevents Aβ25-35-evoked tau protein hyperphosphorylation and apoptosis through JAK2 signaling.

Keywords: Aβ25–35; IL-5; PC12 cells; Tau.

MeSH terms

  • Alzheimer Disease / drug therapy
  • Alzheimer Disease / metabolism
  • Alzheimer Disease / pathology
  • Amyloid beta-Peptides / metabolism*
  • Animals
  • Apoptosis* / drug effects
  • Cell Survival / drug effects
  • Enzyme Activation / drug effects
  • Interleukin-5 / metabolism*
  • Interleukin-5 Receptor alpha Subunit / agonists*
  • Interleukin-5 Receptor alpha Subunit / antagonists & inhibitors
  • Interleukin-5 Receptor alpha Subunit / genetics
  • Interleukin-5 Receptor alpha Subunit / metabolism
  • Janus Kinase 2 / antagonists & inhibitors
  • Janus Kinase 2 / chemistry
  • Janus Kinase 2 / metabolism
  • Nerve Tissue Proteins / agonists
  • Nerve Tissue Proteins / antagonists & inhibitors
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism
  • Neurons / drug effects
  • Neurons / metabolism*
  • Neurons / pathology
  • PC12 Cells
  • Peptide Fragments / metabolism*
  • Phosphorylation / drug effects
  • Protein Kinase Inhibitors / pharmacology
  • Protein Processing, Post-Translational* / drug effects
  • Pyrrolidines / pharmacology
  • RNA Interference
  • Rats
  • Signal Transduction / drug effects
  • Sulfonamides / pharmacology
  • tau Proteins / metabolism*

Substances

  • Amyloid beta-Peptides
  • Interleukin-5
  • Interleukin-5 Receptor alpha Subunit
  • Mapt protein, rat
  • Nerve Tissue Proteins
  • Peptide Fragments
  • Protein Kinase Inhibitors
  • Pyrrolidines
  • Sulfonamides
  • amyloid beta-protein (25-35)
  • tau Proteins
  • Fedratinib
  • Jak2 protein, rat
  • Janus Kinase 2