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K‐252a‐induced polyploidization and differentiation of a human megakaryocytic cell line, Meg‐J: transient elevation and subsequent suppression of cyclin B 1 and cdc2 expression in the process of polyploidization
Author(s) -
Iwabe Koji,
Teramura Masanao,
Yoshinaga Kentaro,
Kobayashi Shoko,
Hoshikawa Yutaka,
Maeda Tatsuya,
Hatakeyama Masanori,
Mizoguchi Hideaki
Publication year - 1998
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.1365-2141.1998.00819.x
Subject(s) - transient (computer programming) , cell culture , cyclin , cyclin dependent kinase 1 , line (geometry) , microbiology and biotechnology , biology , cancer research , cell cycle , cell , genetics , computer science , mathematics , geometry , operating system
Megakaryocytes are unique haemopoietic cells which undergo DNA replication, giving rise to polyploid cells. However, little is known about the mechanism of megakaryocytic polyploidization. To address this issue, we used the human megakaryocytic cell line Meg‐J. In the presence of K‐252a (an indolocarbasole derivative), Meg‐J cells stopped proliferation and exhibited additional megakaryocytic features, including morphological changes, polyploidization, and increases in the levels of surface expression of platelet glycoprotein (GP) IIb/IIIa and GPIb. Thrombopoietin (TPO) promoted the K‐252a‐induced polyploidization and megakaryocytic differentiation. In the process of K‐252a‐induced polyploidization, levels of expression of both cdc2 and cyclin B 1 were elevated transiently and subsequently decreased. This suggested that the polyploidization process in Meg‐J cells was at least in part associated with a transient elevation and subsequent decrease in the expression of cdc2/cyclin B 1 complex, a critical kinase involved in G2/M cell cycle transition.