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Elimination of the Unnecessary: Intra- and Extracellular Signaling by Anionic Phospholipids
  • Published Date:
    Feb 03 2017
  • Source:
    Biochem Biophys Res Commun. 482(3):482-490.

Public Access Version Available on: February 03, 2018 information icon
Please check back on the date listed above.
  • Pubmed ID:
  • Pubmed Central ID:
  • Description:
    High fidelity of biological systems is frequently achieved by duplication of the essential intracellular machineries or, removal of the entire cell, which becomes unnecessary or even harmful in altered physiological environments. Carefully controlled removal of these cells, without damaging normal cells, requires precise signaling, and is critical to maintaining homeostasis. This review describes how two anionic phospholipids - phosphatidylserine (PS) and cardiolipin (CL) - residing in distinct compartments of the cell, signal removal of "the unnecessary" using several uniform principles. One of these principles is realized by collapse of inherent transmembrane asymmetry and the externalization of the signal on the outer membrane surface - mitochondria for CL and the plasma membrane for PS - to trigger mitophagy and phagocytosis, respectively. Release from damaged cells of intracellular structures with externalized CL or externalized PS triggers their elimination by phagocytosis. Another of these principles is realized by oxidation of polyunsaturated species of CL and PS. Highly specific oxidation of CL by cytochrome c serves as a signal for mitochondria-dependent apoptosis, while oxidation of externalized PS improves its effectiveness to trigger phagocytosis of effete cells.

  • Document Type:
  • Collection(s):
  • Funding:
    R01 CA165065/CA/NCI NIH HHS/United States
    R01 ES020693/ES/NIEHS NIH HHS/United States
    R01 OH008282/OH/NIOSH CDC HHS/United States
    U19 AI068021/AI/NIAID NIH HHS/United States
    R01 NS076511/NS/NINDS NIH HHS/United States
    R01 HL094488/HL/NHLBI NIH HHS/United States
    R01 NS061817/NS/NINDS NIH HHS/United States
    P01 HL114453/HL/NHLBI NIH HHS/United States
    R01 NS084604/NS/NINDS NIH HHS/United States
    R21 ES021068/ES/NIEHS NIH HHS/United States
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