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M Tashima

Publications and source records attributed to M Tashima.

At least 55 records · Page 3Linked to original sources
PubMed1987

Magnesium deprivation inhibits the expression of differentiation-related phenotypes in human promyelocytic leukemia HL-60 cells.

The role of magnesium ions in the differentiation of human promyelocytic leukemia HL-60 cells was investigated. When HL-60 extracellular magnesium was deficient (less than 0.01 mM), the total intracellular magnesium content and [3H] leucine incorporation rates decreased to 61 and 28%, respectively, on day 3. When the cells were treated with various inducers (100 nM 1 alpha, 25 dihydroxyitamine D3 (1,25(OH)2D3), 100 nM beta-all-trans retinoic acid (RA), 20 nM 12-o-tetradecanoyl phorbol-13-acetate (TPA), 1.25% dimethylsulfoxide (DMSO) and 30 nM aclacinomycin (AcM] in magnesium-deficient medium, the expression of differentiation-related phenotypes (nitroblue tetrazolium (NBT) reducing ability, nonspecific esterase (NSE) activity and monoclonal antibody, OKM1 binding activity) was almost completely inhibited. After a 2-day treatment with 100 nM 1,25(OH)2D3 in magnesium-deficient medium, the expression of differentiation-related phenotypes was restored by further incubation in the absence of inducer in standard magnesium medium (0.4 mM). These results suggested that magnesium deprivation inhibited the expression of HL-60 differentiation-related phenotypes but not their commitment to differentiation. These phenotypes were expressed without inducer in standard magnesium medium after a 2-day simultaneous treatment with 1,25(OH)2D3 and cyclohexamide (protein synthesis inhibitor) in magnesium-deficient medium, but not after simultaneous pretreatment with 1,25(OH)2D3 and alpha-amanitin (RNA synthesis inhibitor). Thus, it was suggested that the magnesium-requiring step in HL-60 cell differentiation is in protein but not mRNA synthesis. This conclusion is supported by the findings that changes in c-myc and c-fms mRNA levels in HL-60 cells treated with 100 nM 1,25(OH)2D3 in magnesium-deficient medium and those in standard magnesium medium were the same. In addition, dibutyryl cyclic adenosine monophosphate (dbc AMP) could restore expression of differentiation-related phenotypes inhibited by magnesium deprivation but not those inhibited by cyclohexamide, even though magnesium deprivation inhibited protein synthesis as much as did cyclohexamide. This suggests that magnesium-requiring step in HL-60 cell differentiation is different from that inhibited by cyclohexamide.

Aclarubicin↗
PubMed1986

Role of intracellular calcium ion in human promyelocytic leukemia HL-60 cell differentiation.

The relationship between calcium ions and the differentiation of human promyelocytic leukemia HL-60 cells was investigated. Proliferation of HL-60 cells incubated in calcium-free medium was inhibited without cell differentiation. On the other hand, incubation with 100 microM verapamil markedly inhibited cell proliferation and caused slight cell differentiation into monocytes. Both calcium-free medium and 100 microM verapamil enhanced HL-60 cell differentiation after treatment with 1 nM 1 alpha,25-dihydroxyvitamin D3, 1 nM beta-all-trans-retinoic acid, or 0.75% dimethyl sulfoxide. However, no enhancement was obtained by treatment with 1 nM 12-O-tetradecanoylphorbol-13-acetate. The free cytosolic calcium concentration was measured by the intracellularly trappable fluorescent calcium indicator, quin 2. The increase of intracellular calcium induced by 250 nM ionomycin was completely blocked by 100 microM verapamil in calcium-free medium, suggesting that the high concentration of verapamil (100 microM) blocks the intracellular calcium mobilization in HL-60 cells. Therefore, the enhancing effect of calcium deprivation or verapamil of HL-60 cell differentiation seemed to be closely related to the inhibition of intracellular calcium mobilization. This speculation is supported by the finding that 50 microM 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate, an intracellular calcium antagonist, also enhanced HL-60 cell differentiation induced by 1 alpha,25-dihydroxyvitamin D3, beta-all-trans-retinoic acid, or dimethyl sulfoxide.

Calcitriol↗
PubMed1986

[Treatment of atypical leukemia].

Treatment of atypical leukemia is reviewed with emphasis on the establishment of the concept of atypical leukemia and the treatment of this disease is discussed on a historical basis. Furthermore, a recent approach to this disease based on induction of differentiation of leukemia cells by low-dose cytosine arabinoside is discussed.

Aged↗
PubMed1985

Effect of antimetabolites and thymidine blockage on the induction of differentiation of HL-60 cells by retinoic acid or 1 alpha,25-dihydroxyvitamin D3.

Induction of differentiation of the HL-60 human promyelocytic leukemia cell line by retinoic acid or 1 alpha,25(OH)2D3 was analyzed under the condition in which cellular DNA synthesis was inhibited by several antimetabolites or blocked by thymidine. The results demonstrate that differentiation occurs in the absence of DNA synthesis and that some inhibitors of DNA synthesis may enhance the differentiation of HL-60 cells by the above inducers. Among the antimetabolites used, the enhancement of induction of differentiation by hydroxyurea was shown to be more effective than that of Ara-C or aphidicolin. The effect of thymidine blockage was similar to that of hydroxyurea. These different effects may be due to the different points at which the cell cycle is blocked by these agents. These results seem to be common in both the differentiation of the granulocytic line induced by retinoic acid and of the macrophage line induced by 1 alpha,25(OH)2D3. The present study also suggests that combination treatment with the inhibitor of DNA synthesis and the inducer of differentiation could be beneficial in the clinical therapy of leukemia. The mode of action of clinical low-dose Ara-C treatment is also discussed.

Antibiotics, Antineoplastic↗
PubMed1981

Presence of a highly repetitive and widely dispersed DNA sequence in the human genome.

A genomic DNA library consisting of human DNA fragments about 18 kilobases long cloned in a bacteriophage lambda vector was found to contain a specific repeated DNA segment. The repeated sequence is present in greater than 95% of the genomic library, and selected clones contain at least two copies of the sequence. Our experiments indicate that this highly repetitive sequence (approximately 400,000 copies per haploid genome) is widely distributed in the human genome and is represented in the cytoplasmic polysomal mRNA. This sequence is homologous to the 300-base-pair Alu repeat family, the predominant repeat sequence in man.

Cloning, Molecular↗
PubMed1980

Myelofibrosis with skin lesions.

An elderly male patient with primary myelofibrosis developed many papules on the trunk and later numerous subcutaneous nodules on the face. Histologically these lesions showed the features of extra-medullary haematopoiesis consisting of all the three components, i.e. myeloid, erythroid and megakaryocytic elements, findings never reported in the skin.

Aged↗