Transfusion Medicine Reviews
Volume 22, Issue 4 , Pages 268-279, October 2008

Platelet Storage Lesion: A New Understanding From a Proteomic Perspective

  • Jonathan N. Thon
  • ,
  • Peter Schubert
  • ,
  • Dana V. Devine

      Affiliations

    • Corresponding Author InformationAddress reprint requests to Dana Devine, PhD, Vice President, Medical, Scientific and Research Affairs, Canadian Blood Services, UBC Centre for Blood Research, 4th Floor, 2350 Health Sciences Mall, Vancouver, BC, Canada V6T 1Z3.

Canadian Blood Services, Vancouver, BC, Canada

Department of Biochemistry and Molecular Biology, University of British Columbia, Vancouver, BC, Canada

Centre for Blood Research, University of British Columbia, Vancouver, BC, Canada

Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada

Platelet storage and availability for the purposes of transfusion are currently restricted by a markedly short shelf life of 5 to 7 days owing to an increased risk of bacterial growth and storage-related deterioration called the platelet storage lesion. Because most bacteria grow to confluence within 5 days during storage at room temperature, there is little increased risk of bacterial overgrowth with testing in place, and the only remaining issue is the quality of platelets during the extended storage. Although the manifestations of the storage lesion have been well studied using a variety of in vitro measures, the precise biochemical pathways involved in the initiation and progression of this process have yet to be identified. Proteomics has emerged as a powerful tool to identify and monitor changes during platelet storage and, in combination with biochemical and physiologic studies, facilitates the development of a sophisticated mechanistic view. In this review, we summarize recent experimental work that has led to a detailed overview of protein changes linked to platelet functions and signaling pathways, providing potential targets for inhibitors to ameliorate the storage lesion.

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 JNT and PS contributed equally to this work.

PII: S0887-7963(08)00040-0

doi:10.1016/j.tmrv.2008.05.004

Transfusion Medicine Reviews
Volume 22, Issue 4 , Pages 268-279, October 2008