Appetizing Rancidity of Apoptotic Cells for Macrophages: Oxidation, Externalization, and Recognition of Phosphatidylserine

Details

• Personal Author:
  Borisenko GG ; Fabisiak JP ; Fadeel B ; Jiang J ; Kagan VE ; Liu SX ; Serinkan BF ; Shvedova AA ; Tyurin VA ; Tyurina YY ; Uthaisang W
• Description:
  Programmed cell death (apoptosis) functions as a mechanism to eliminate unwanted or irreparably damaged cells ultimately leading to their orderly phagocytosis in the absence of calamitous inflammatory responses. Recent studies have demonstrated that the generation of free radical intermediates and subsequent oxidative stress are implicated as part of the apoptotic execution process. Oxidative stress may simply be an unavoidable yet trivial byproduct of the apoptotic machinery; alternatively, intermediates or products of oxidative stress may act as essential signals for the execution of the apoptotic program. This review is focused on the specific role of oxidative stress in apoptotic signaling, which is realized via phosphatidylserine-dependent pathways leading to recognition of apoptotic cells and their effective clearance. In particular, the mechanisms involved in selective phosphatidylserine oxidation in the plasma membrane during apoptosis and its association with disturbances of phospholipid asymmetry leading to phosphatidylserine externalization and recognition by macrophage receptors are at the center of our discussion. The putative importance of this oxidative phosphatidylserine signaling in lung physiology and disease are also discussed. [Description provided by NIOSH]
• Subjects:
  Free Radicals Lung Occupational Health Respiratory System Safety
• Keywords:
  Apoptosis Author Keywords: Phosphatidylserine Oxidation And Externalization Cell-morphology Cytochrome C Free-radicals Lung-function Macrophage Receptor Oxidative-processes Phagocytic-activity Phagocytosis Plasma-membrane

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• ISSN:
  1040-0605
• Document Type:
  Text
• Genre:
  Journal Article
• Place as Subject:
  OSHA Region 3 ; Pennsylvania ; West Virginia
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Division:
  HELD - Health Effects Laboratory Division
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Volume:
  285
• Issue:
  1
• NIOSHTIC Number:
  nn:20023022
• Citation:
  Am J Physiol Lung Cell Mol Physiol 2003 Jul; 285(1):L1-L17
• Contact Point Address:
  V. E. Kagan, Dept. of Environmental and Occupational Health, Univ. of Pittsburgh, Pittsburgh, PA 15260
• Email:
  kagan@pitt.edu
• Federal Fiscal Year:
  2003
• NORA Priority Area:
  Disease and Injury: Allergic and Irritant Dermatitis
• Peer Reviewed:
  True
• Source Full Name:
  American Journal of Physiology: Lung Cellular and Molecular Physiology
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:eb39183497b5f3cc38dd68769ac1824d02272ee800ba97a088428c6e19720e751cabb571b4c7d9fad4fd07579f126d5409b783309f0b54dbac2ff60c348ce444
• Download URL:
  https://stacks.cdc.gov/view/cdc/199612/cdc_199612_DS1.pdf
• File Type:
  [PDF - 713.67 KB ]