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The effects of anagrelide on human megakaryocytopoiesis
Author(s) -
Solberg Jr Lawrence A.,
Tefferi Ayalew,
Oles Karl J.,
Tarach Jerzy S.,
Petitt Robert M.,
Forstrom Lee A.,
Silverstein Murray N.
Publication year - 1997
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1997.3503164.x
Subject(s) - anagrelide , megakaryocytopoiesis , platelet , in vivo , megakaryocyte , medicine , progenitor cell , pharmacology , in vitro , cancer research , essential thrombocythemia , andrology , endocrinology , biology , stem cell , microbiology and biotechnology , genetics
Anagrelide, an inhibitor of platelet aggregation, decreases the number of platelets in normal subjects and in patients with myeloproliferative disorders. We describe studies aimed at discovering the general mechanism(s) by which anagrelide acts. We examined three hypotheses: (1) anagrelide shortens platelet survival, (2) anagrelide inhibits the proliferation of megakaryocytic‐committed progenitor cells (CFU‐M), and (3) anagrelide inhibits maturation of megakaryocytes. We observed that anagrelide did not shorten platelet survival. Proliferation of CFU‐M in vivo was not affected by anagrelide, although high concentrations of anagrelide inhibited CFU‐M in vitro . In‐vivo and in‐vitro anagrelide altered the maturation of megakaryocytes, causing a decrease in their size and changing other morphometric features. We conclude that anagrelide decreases the number of platelets primarily by interfering with the maturation of megakaryocytes.