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The phospholipase A2 pathway controls a synaptic cholesterol ester cycle and synapse damage.

Craig Osborne1, Ewan West1, Clive Bate2

  • 1Department of Pathology and Pathogen Biology, Royal Veterinary College, Hawkshead Lane, North Mymms, Hatfield, UK AL9 7TA.

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|March 29, 2018
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Summary

Platelet activating factor (PAF) regulates cholesterol metabolism and signaling complex formation in synapses. This process influences synapse degeneration by controlling cytoplasmic phospholipase A2 (cPLA2) and cyclooxygenase-2 (COX-2) activation.

Keywords:
CholesterolCyclooxygenaseEsterificationPhospholipase A2Platelet-activating factorSynaptosome

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Cell Biology

Background:

  • Cellular prion protein (PrPC) organizes signaling complexes in synaptosomes.
  • Amyloid-β (Aβ) oligomers aggregate PrPC, activating cytoplasmic phospholipase A2 (cPLA2) and leading to synapse degeneration.
  • Synaptic signaling platforms rely on cholesterol released by cholesterol ester hydrolases (CEHs).

Purpose of the Study:

  • To investigate the role of platelet activating factor (PAF) in regulating synaptic signaling complexes.
  • To elucidate the mechanisms of signaling complex dispersal and cessation of signaling.
  • To understand the involvement of cholesterol esterification in synapse protection.

Main Methods:

  • Investigated the formation and dispersal of Aβ-PrPC-cPLA2 signaling complexes.
  • Examined the role of PAF in the recruitment of Fyn and COX-2.
  • Studied the effect of acyl-coenzyme A:cholesterol acyltransferase (ACAT)-1 on cholesterol levels and complex stability.

Main Results:

  • A positive feedback loop exists where activated cPLA2 increases cholesterol, further activating cPLA2.
  • PAF is crucial for incorporating Fyn and COX-2 into signaling complexes.
  • PAF-mediated recruitment of ACAT-1 esterifies cholesterol, dispersing complexes and halting signaling.

Conclusions:

  • PAF is a key regulator of the cholesterol ester cycle, cPLA2, and COX-2 activation in synapses.
  • Cholesterol esterification by ACAT-1 is essential for dispersing signaling complexes and preventing synapse damage.
  • Understanding these mechanisms offers insights into synapse degeneration and potential therapeutic targets.