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5‐azacytidine supports the long‐term repopulating activity of cord blood CD34 + cells
Author(s) -
Suzuki Motoyuki,
Harashima Akira,
Okochi Ayumi,
Yamamoto Mayuko,
Nakamura Shuji,
Motoda Ryuichi,
Yamasaki Fumiyuki,
Orita Kunzo
Publication year - 2004
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.20178
Subject(s) - dna methylation , haematopoiesis , cord blood , biology , progenitor cell , dna demethylation , methylation , demethylating agent , azacitidine , cd34 , demethylation , epigenetics , embryonic stem cell , microbiology and biotechnology , stem cell , dna , immunology , genetics , gene expression , gene
DNA methylation plays important roles in a wide range of biological phenomena, especially in the embryonic development and tumorigenesis. However, correlations between differentiation and DNA methylation have not been clarified well in each differentiation system. In this study, we focused our attention on regulatory roles of DNA methylation in normal hematopoietic differentiation using a demethylating reagent, 5‐azacytidine (5‐AzaC). As a source of hematopoietic progenitor cells, we used CD34 + cells prepared from human umbilical cord blood and examined the effects of 5‐AzaC on the colony‐forming activity and the long‐term culture‐initiating (LTC‐IC) activity of these cells. 5‐AzaC treatment increased LTC‐IC frequency 1.57‐ to 2.50‐fold as compared to the nontreated control. In parallel to this, immunoblotting analysis showed that the intensity of overall DNA methylation decreased after 5‐AzaC treatment. These results indicated the involvement of DNA methylation and demethylation in controlling immaturity of hematopoietic progenitor cells and the usefulness of 5‐AzaC for regulating this immaturity. Am. J. Hematol. 77:313–315, 2004. © 2004 Wiley‐Liss, Inc.