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Blood, 1 September 2006, Vol. 108, No. 5, pp. 1429.
Proplatelet formation: IIb or not IIb?UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
Findings by Larson and Watson suggest a role for platelet GPIIb in murine proplatelet formation through a mechanism that is independent of classic outside-in integrin signaling networks.
Growing evidence suggests that platelets are generated from megakaryocytes through the formation of cytoplasmic extensions called proplatelets. Mature platelets are released from the ends of the proplatelets, and proplatelet extensions undergo extensive branching that increases the number of ends available for platelet release.2 Recent reports have shown that proplatelet extensions have a complex and highly ordered structure that allows them to function much like a railway system transporting platelet contents from the body of the megakaryocytes to the distal, maturing platelets.3 Despite such elegant cell biology, we remain largely uninformed regarding what triggers and regulates proplatelet formation.
Using simple in vitro proplatelet assays, Larson and Watson observed that fibrinogen-coated surfaces promote megakaryocyte proplatelet formation, whereas laminin-, vitro-nectin-, and collagen-coated surfaces do not. Proplatelet formation on fibrinogen-coated surfaces was significantly reduced in the presence of an
While
Larson and Watson remind us that developing hematopoietic cells, and not just stem cells, have an environment that plays a functional role in the biology of the cell, and, like most interesting work, their report raises more questions than it answers. What is the biologic significance of their findings? Why do patients with Glanzmann thrombasthenia have normal platelet counts? Is the fibrinogen- References
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| Copyright © 2006 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||||
IIb, GPIIb plays a critical role in hemostasis through its function as the primary platelet fibrinogen receptor, has been a popular and successful target for antiplatelet drugs, and its absence leads to the inherited bleeding disorder Glanzmann thrombasthenia. Larson and Watson suggest that 
3 antagonist or blocking antibody, and they were not detectable in megakaryocytes from 
2-/- murine megakaryocytes formed proplatelets on fibrinogen-coated surfaces more efficiently than did wild-type megakaryocytes, and inhibition of intracellular Ca++ elevation did not diminish fibrinogen-induced proplatelet formation, yet all of these maneuvers are expected to impair classic integrin outside-in signaling. 
