Thrombopoietin production in mice treated with acetylsalicylic acid.
Recent work revealed that mice in which platelet function was inhibited by acetylsalicylic acid (ASA) treatment showed evidence of increased platelet production. It was proposed that poorly functioning platelets gave rise to elevated thrombocytopoiesis by causing the release and action of thrombopoietin. However, direct evidence is lacking. Therefore, in the work reported here, plasma from mice treated with ASA was injected into normal recipient mice in an attempt to document the existence of the humoral factor. Compared with control mice given normal plasma, the injection of mice with plasma from ASA-treated mice resulted in increased thrombocytopoiesis, as evidenced by significant increases in the percentage of 35S incorporation into platelets, larger platelet size, and elevated megakaryocyte precursor cells (the small acetylcholinesterase-positive cell). For a positive control, additional mice were treated with plasma from animals made thrombocytopenic by an injection of antiplatelet serum. These mice also showed significant increases in thrombocytopoiesis. The results support the hypothesis that platelet production in ASA-treated mice is elevated by release and action of thrombopoietin.
Clift
R E
RE
Department of Animal Science, College of Veterinary Medicine, University of Tennessee, Knoxville 37901-1071.
Cottrell
M B
MB
McDonald
T P
TP
D000818:Animals; D001241:Aspirin / Q000494:pharmacology*; D001792:Blood Platelets / Q000166:cytology / Q000378:metabolism; D002455:Cell Division / Q000187:drug effects; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D015539:Platelet Activation / Q000187:drug effects / Q000502:physiology; D013926:Thrombopoietin / Q000096:biosynthesis*
D013926:Thrombopoietin; D001241:Aspirin