Platelet senescence is regulated by an internal timer, not damage inflicted by hits
Details
Publication Year 2010-09-09,Volume 116,Issue #10,Page 1776-1778
Journal Title
BLOOD
Publication Type
Journal Article
Abstract
The mechanisms responsible for the brief life span of blood platelets have been a subject of speculation since the 1950s. The most popular hypothesis to date has been the "multiple-hit" model, whereby damage inflicted by external "hits" triggers recognition and clearance by the reticuloendothelial system. Recently, it was demonstrated that platelets contain an apoptotic pathway that mediates their survival in vivo. Using a novel labeling technique to measure population and cohort survival in mice carrying mutations in this pathway, combined with mathematical modeling, we have studied the internal and external control of platelet fate. Our results cast doubt on the veracity of the multiple-hit model. An alternative model, under which platelets are born with an internal "timer," provides a more parsimonious interpretation of the data. Thus, at steady state, platelet senescence is probably the product of internal processes rather than external hits. (Blood. 2010; 116(10):1776-1778)
Publisher
AMER SOC HEMATOLOGY
Keywords
LIFE-SPAN; BLOOD-PLATELETS; SIALIC-ACID; IN-VIVO; SIZE; SURVIVAL; AGE; KINETICS; MODEL; CIRCULATION
Research Division(s)
Immunology; Molecular Medicine
Terms of Use/Rights Notice
© 2010 by The American Society of Hematology


Creation Date: 2010-09-09 12:00:00
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