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2014 ; 13
(24
): 3938-47
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2-Arachidonoylglycerol enhances platelet formation from human megakaryoblasts
#MMPMID25427281
Gasperi V
; Avigliano L
; Evangelista D
; Oddi S
; Chiurchiù V
; Lanuti M
; Maccarrone M
; Valeria Catani M
Cell Cycle
2014[]; 13
(24
): 3938-47
PMID25427281
show ga
Platelets modulate vascular system integrity, and their loss is critical in
haematological pathologies and after chemotherapy. Therefore, identification of
molecules enhancing platelet production would be useful to counteract
thrombocytopenia. We have previously shown that 2-arachidonoylglycerol (2-AG)
acts as a true agonist of platelets, as well as it commits erythroid precursors
toward the megakaryocytic lineage. Against this background, we sought to further
interrogate the role of 2-AG in megakaryocyte/platelet physiology by
investigating terminal differentiation, and subsequent thrombopoiesis. To this
end, we used MEG-01 cells, a human megakaryoblastic cell line able to produce in
vitro platelet-like particles. 2-AG increased the number of cells showing ruffled
surface and enhanced surface expression of specific megakaryocyte/platelet
surface antigens, typical hallmarks of terminal megakaryocytic differentiation
and platelet production. Changes in cytoskeleton modeling also occurred in
differentiated megakaryocytes and blebbing platelets. 2-AG acted by binding to
CB1 and CB2 receptors, because specific antagonists reverted its effect.
Platelets were split off from megakaryocytes and were functional: they contained
the platelet-specific surface markers CD61 and CD49, whose levels increased
following stimulation with a natural agonist like collagen. Given the importance
of 2-AG for driving megakaryopoiesis and thrombopoiesis, not surprisingly we
found that its hydrolytic enzymes were tightly controlled by classical inducers
of megakaryocyte differentiation. In conclusion 2-AG, by triggering megakaryocyte
maturation and platelet release, may have clinical efficacy to counteract
thrombocytopenia-related diseases.
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