Immobilized amyloid Aβ peptides support platelet adhesion and activation

FEBS Lett. 2013 Aug 19;587(16):2606-11. doi: 10.1016/j.febslet.2013.06.041. Epub 2013 Jul 4.

Abstract

Accumulation of amyloidogenic Aβ peptides in the brain contributes to the onset of Alzheimer disease. Aβ peptide deposits are also present in blood vessel walls, mainly deriving from circulating platelets. However, their effect on platelet function is unclear. We demonstrate that immobilized Aβ peptides induce platelet adhesion and spreading through metalloproteinase-sensitive surface receptors. Aβ peptides also fasten platelet spreading on collagen, and support the time- and ADP-dependent activation of adherent platelets, leading to stimulation of several signalling proteins. Our results indicate a potential role for peripheral Aβ peptides in promoting platelet adhesion and activation in the initiation of thrombus formation.

Keywords: AD; APP; Adhesion; Alzheimer disease; Amyloid Aβ peptide; Cerebrovascular inflammation; Human platelet; PI3K; PKC; PLC; amyloid precursor protein; phosphatidylinositol 3 kinase; phospholipase C; protein kinase C.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Diphosphate / metabolism
  • Alzheimer Disease / metabolism
  • Amyloid beta-Peptides / metabolism*
  • Blood Vessels / metabolism
  • Cell Adhesion
  • Cell Membrane / metabolism
  • Cerebrovascular Disorders / blood
  • Cerebrovascular Disorders / metabolism
  • Collagen / metabolism
  • Humans
  • Immobilized Proteins / metabolism
  • Metalloproteases / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism
  • Platelet Activation*
  • Platelet Adhesiveness*
  • Protein Kinase C / metabolism
  • Thrombosis / metabolism

Substances

  • Amyloid beta-Peptides
  • Immobilized Proteins
  • Adenosine Diphosphate
  • Collagen
  • Phosphatidylinositol 3-Kinases
  • Protein Kinase C
  • Metalloproteases