Intrinsic apoptosis circumvents the functional decline of circulating platelets but does not cause the storage lesion

Author:

Pleines Irina123ORCID,Lebois Marion1,Gangatirkar Pradnya1,Au Amanda E.12,Lane Rachael M.14,Henley Katya J.1,Kauppi Maria12,Corbin Jason1,Cannon Ping1,Bernardini Jonathan12,Alwis Imala56ORCID,Jarman Kate E.12,Ellis Sarah78,Metcalf Donald1,Jackson Shaun P.569ORCID,Schoenwaelder Simone M.56ORCID,Kile Benjamin T.124ORCID,Josefsson Emma C.12ORCID

Affiliation:

1. The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia;

2. Department of Medical Biology, The University of Melbourne, Melbourne, VIC, Australia;

3. Institute of Experimental Biomedicine, University Hospital and Rudolf Virchow Center Würzburg, Germany;

4. Anatomy and Developmental Biology, Monash Biomedicine Discovery Institute, Monash University, Clayton, VIC, Australia;

5. Heart Research Institute, Newtown, NSW, Australia;

6. Charles Perkins Centre, The University of Sydney, Camperdown, NSW, Australia;

7. Cancer Research Division, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia;

8. Sir Peter MacCallum Department of Oncology, University of Melbourne, Melbourne, VIC, Australia; and

9. Department Cardiology, Royal Prince Alfred Hospital, Camperdown, NSW, Australia

Abstract

Key Points BAK/BAX depletion in murine platelets reveals that intrinsic apoptosis is not required for the development of the platelet storage lesion. Restriction of platelet life span by intrinsic apoptosis is pivotal to maintain a functional, hemostatically reactive platelet population.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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