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CW Jackson, NK Hutson, SA Steward, RA Ashmun, DS Davis, HH Edwards, JE Rehg and ME Dockter
Department of Hematology/Oncology, St Jude Children's Research Hospital,
Memphis, TN.
The mechanisms that determine and regulate platelet size are unknown. By
phase microscopy, we observed that Wistar Furth (WF) rats had
macrothrombocytopenia. In this study, we have characterized and compared
platelets and megakaryocytes of WF rats with those of Wistar, Long-Evans
hooded (LE), and Sprague-Dawley rats. In addition, we have examined the
mode of inheritance of this WF rat platelet abnormality. The average
platelet count of WF rats was only one-third that of the other three rat
strains. In contrast, the mean platelet volume (MPV) of adult WF rats was
twice that of the other rat strains; however, the average megakaryocyte
diameter and DNA content distribution of WF rats were not significantly
different from those of LE rats. The average megakaryocyte concentration
was 30% lower in the WF strain compared with that of LE rats. Mazelike
membrane formations were observed in WF platelets and megakaryocytes by
electron microscopy. Reciprocal crosses of WF and LE rats resulted in
offspring with MPVs and platelet counts like those of LE rats, indicating
that the macrothrombocytopenic trait is recessive in its inheritance.
Reciprocal marrow transplants between the WF and LE strains resulted in
MPVs like those of the donor strain, demonstrating that the
macrothrombocytopenia is an intrinsic marrow abnormality of the WF strain.
Splenectomy did not alter the MPV of WF rats. The response of WF
megakaryocytes and platelets to severe, acute thrombocytopenia was similar
to that of LE rats except that the shift to higher megakaryocyte DNA
contents was muted and platelet recovery was slower in the WF rats. In
summary, the WF rat has a hereditary macrothrombocytopenia that is
recessive in nature and not due to differences in megakaryocyte size or DNA
content. These results suggest that the macrothrombocytopenia of WF rats
results from the formation of fewer platelets per megakaryocyte, possibly
resulting from a qualitative or quantitative defect in some component
necessary for proper subdivision of megakaryocyte cytoplasm into platelets.
This article has been cited by other articles:
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| Copyright © 1988 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||