5-Aminolevulinate Synthase Expression and Hemoglobin Synthesis in a Human Myelogenous Leukemia Cell Line.

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  • Nagai Tadashi
    Department of Biochemistry and Tohoku University School of Medicine Laboratory of Biochemical Hematology, The Rockefeller University
  • Harigae Hideo
    Department of Biochemistry and Tohoku University School of Medicine Department of Internal Medicine, Tohoku University School of Medicine
  • Furuyama Kazumichi
    Department of Biochemistry and Tohoku University School of Medicine
  • Munakata Hiroshi
    Department of Biochemistry and Tohoku University School of Medicine
  • Hayashi Norio
    Department of Biochemistry and Tohoku University School of Medicine
  • Endo Kazuyasu
    Department of Internal Medicine, Tohoku University School of Medicine
  • Sassa Shifferu
    Laboratory of Biochemical Hematology, The Rockefeller University
  • Yamamoto Macavnki
    Center for Tsukuba Advanced Research Allian and Institute of Basic Medical Sciences, University of Tsukuba

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  • 5 Aminolevulinate Synthase Expression a

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We examined the effect of hemin, TGF-β1 and cytosine arabinoside (Ara-C) on the levels of mRNAs for the erythroid-specific 5-aminolevulinate synthase (ALAS-E) and γ-globin in various human myelogenous leukemia cell lines. Detailed analyses were also made using one of them, YN-1, which was isolated and established in culture from a patient with chronic myelogenous leukemia. Our results demonstrate that γ-globin protein level and the percentage of benzidine-positive cells in the cell line increased markedly (10- to 30-fold) upon treatment with hemin, TGF-β1, or Ara-C. In contrast, γ-globin mRNA was already markedly expressed prior to treatment in 4 out of 9 cell lines examined, including YN-1, and the level increased only marginally after treatment with hemin. ALAS-E mRNA levels were increased in YN-1 cells after treatment with TGF-β1 and Ara-C, while hemin treatment had little effect. These results indicate that heme supply is insufficient in YN-1 cells and suggest that hemin increases hemoglobin synthesis principally at the post-tran-scriptional level, whereas TGF-β1 and Ara-C stimulate hemoglobin synthesis by activating efficient endogenous heme supply in the cells.

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