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Biomedical subjects

T Takimoto

Publications and source records attributed to T Takimoto.

At least 127 records · Page 7Linked to original sources
PubMed1988

Changes in sensitivity to anticancer drugs during TPA-induced cellular differentiation in a human T-lymphoblastoid cell line (MOLT-4).

After four days of treatment with 10(-8) M TPA, differentiation of the human T-lymphoblastoid cell line MOLT-4 was induced along the T cell lineage, confirmed by a fall in adenosine deaminase and 5'-ectonucleotidase and a rise in purine nucleoside phosphorylase activity. TPA-treated cells became resistant to the cytotoxic effects of 1-beta-D-arabinofuranosylcytosine (Ara-C), 9-beta-D-arabinofuranosyladenine (Ara-A), and 2-chlorodeoxyadenosine. This was, in part, due to the altered cell cycle distribution (accumulation of cells in the G1 phase), since the toxicity of Ara-C and Ara-A is S phase specific. The diminished rate of Ara-C transport concomitant with Ara-CTP formation after TPA treatment is considered to be the biochemical basis for this acquired resistance.

Antineoplastic Agents↗
PubMed1987

Prevention of adriamycin-induced interphase death by 3-aminobenzamide and nicotinamide in a human promyelocytic leukemia cell line.

Adriamycin caused significant interphase death in HL-60 cells during six hours of incubation, which was abolished by the poly(ADP-ribose) polymerase inhibitors, 3-aminobenzamide or nicotinamide. Neither agent changed adriamycin uptake by HL-60 cells. Although 3-aminobenzamide did not alter the number of DNA strand breaks caused by adriamycin, it prevented adriamycin-induced depletion of intracellular NAD+ and ATP, and maintained energy charge. These findings suggest that the activation of poly(ADP-ribose) synthesis plays an important role in the adriamycin-induced interphase death of proliferating HL-60 cells.

Benzamides↗
PubMed1987

Cell fusion by nasopharyngeal carcinoma-derived Epstein-Barr virus.

Cell fusion experiments using Epstein-Barr virus (EBV) obtained from nasopharyngeal carcinoma (NPC) hybrid cells (NPC-KT) were carried out to examine whether human adenoid epithelial cells (Ad-AH) could be fused with lymphoblastoid cells (BJAB, Raji, and A2L) superinfected or infected by EBV, and if Ad-AH nuclei of the fused cells could express EBV-associated nuclear antigen. The presence of NPC EBV could induce EBV early antigen in all three lymphoblastoid cell lines. By autoradiography, we found that NPC EBV could induce cell fusion between Ad-AH cells and tritiated thymidine-labeled lymphoblastoid cells. In addition, we found that Ad-AH nuclei of the fused cells expressed EBV-associated nuclear antigen four days after NPC EBV-mediated cell fusion of Ad-AH cells with lymphoblastoid cells.

Antigens, Viral, Tumor↗
PubMed1987

Effect of 12-O-tetradecanoylphorbol-13-acetate (TPA) on Epstein-Barr virus (EBV)-infected cells.

We have examined if 12-O-tetradecanoylphorbol-13-acetate (TPA) enhances soft agar clonability in Epstein-Barr virus (EBV)-infected cells on the basis of interaction between EBV and TPA. When primary human cord blood lymphocytes (HUCLs) were exposed to two different strains of EBV (B95-8 and NPC-KT) and seeded in soft agar medium containing TPA (0.25 ng/ml), it was observed that the number of transformed colonies increased. However, TPA did not enhance the number of colonies in two EBV genome-positive epithelial hybrid cell lines (NPC-KT and D98/HR-1).

Cell Line↗
PubMed1987

Establishment of an Epstein-Barr virus (EBV) genome-positive subline of Ramos (Ramos/NPC) following infection of Ramos with nasopharyngeal carcinoma (NPC)-derived EBV.

An Epstein-Barr virus (EBV) genome-positive epithelial hybrid cell line, NPC-KT, derived from the fusion of primary nasopharyngeal carcinoma cells with a human epithelial cell line of adenoid origin has previously been described (Takimoto, Kamide, and Umeda, 1984a; Takimoto, Ogura, Sato, and Hatano, 1984b; Takimoto, Ogura, Sato, Umeda, and Hatano, 1985). The NPC-KT cells produce virus (NPC virus) with both transforming and lytic properties. An EBV genome-negative human lymphoblastoid cell line, Ramos, was infected with NPC virus. Three months after infection, more than 90% of the cell population expressed EBV-associated nuclear antigen (EBNA). Approximately 40% of the cells exhibited a brilliant pattern, whereas the remaining 50% of the cells showed a faint granular pattern. The result suggests that there may be heterogeneity in NPC virus.

Antigens, Viral↗
PubMed1987

Transfection of human nasopharyngeal epithelial cells with Epstein-Barr virus DNA.

Transfection experiments using Epstein-Barr virus (EBV) DNA were carried out to examine whether three different epithelial cell lines (Ad-AH, D98, and KB) could be transfected and whether biologically active virus could be recovered. We found that the Ad-AH cells derived from the human nasopharynx were more transfectable, as determined by the synthesis of EBV-specific antigens. Concentrates of supernatant fluids obtained from transfected Ad-AH cells were capable of transforming human cord blood lymphocytes (HCBLs). However, no concentrates of supernatant fluids obtained from transfected epithelial cell lines outside the nasopharynx (D98 and KB) were capable of transforming HCBLs.

Cell Line↗
PubMed1987

Marmoset lymphoblastoid cells transformed by NPC-KT-derived Epstein-Barr virus which possesses transforming and superinfecting characteristics.

New world monkey (cotton-top marmoset; CTM) lymphocytes were transformed by two different strains of Epstein-Barr virus (EBV) derived from human nasopharyngeal epithelial/hybrid cells (NPC-KT and A2L/AH). M-KT cells were a CTM lymphoblastoid cell line which was transformed by EBV derived from NPC-KT cells (NPC-KT EBV). M-BA2L cells were a CTM lymphoblastoid cell line which was transformed by EBV derived from A2L/AH cells (A2L/AH EBV). EBV obtained from M-KT cells, like parental NPC-KT EBV, could transform human cord blood lymphocytes (HCBLs) and superinfect Raji cells. EBV obtained from M-BA2L cells, like parental A2L/AH EBV, could transform HCBLs but could not superinfect Raji cells. We have compared the EBV-DNA associated with M-KT cells to NPC-KT EBV-DNA. The results obtained using a DNA restriction enzyme (Hind III) showed that virus DNA prepared from NPC-KT cells is different from EBV-DNA prepared from CTM lymphocytes transformed by EBV derived from infectious mononucleosis (B95-8), but that virus DNA prepared from M-KT cells is identical with parental NPC-KT EBV. These results indicate the possibility that a single NPC-KT EBV is associated with two biological activities.

Animals↗
PubMed1987

Thyroid antigen-antibody nephritis: possible involvement of fucosyl-GM1 as the antigen.

Hyperthyroidism, microscopic hematuria, and proteinuria developed in an 11-year-old girl. Proteinuria decreased during treatment of hyperthyroidism with an antithyroid drug. On admission, serum anti-thyroglobulin antibody, antimicrosomal antibody, and immune complex were present. The thyrotropin binding inhibitory immunoglobulin (TBII) level was low. On the other hand, an antibody to the ganglioside component (fucosyl-GM1) was detected by an enzyme linked immunosolvent assay (ELISA). A thyroid biopsy specimen showed massive lymphocytic infiltration and interstitial fibrosis. A renal biopsy specimen showed marked proliferation of mesangial cells and increased mesangial matrix with focal segmental capillary wall abnormality. Electron microscopec studies demonstrated mild paramesangial dense deposits. By indirect immunofluorescence, granular glomerular basement membrane and mesangial staining were not detected with rabbit antibody to thyroglobulin, but were detected with rabbit antibody to fucosyl GM1. Fucosyl GM1 was also seen along the basilar aspect of the thyroid follicular epithelial cells. These observation suggests the development of glomerulonephritis mediated by thyroid antigen, particularly ganglioside component.

Antigen-Antibody Complex↗
PubMed1986

Primary EBV infection of human umbilical cord lymphocytes and EBV genome-negative lymphoblastoid cell lines (BJAB and Ramos).

The appearance of Epstein-Barr virus (EBV)-associated nuclear antigen (EBNA) and induction of EBV-induced early antigen (EA) in human umbilical cord blood lymphocytes (HUCLs) and two EBV genome-negative Burkitt's lymphoma (BL) lines (BJAB and Ramos) were studied by infection with EBVs prepared from three different cell lines: marmoset cell line (B95-8) derived from infections mononucleosis, BL-derived cell line (P3HR-1) and human epithelial hybrid cell line (NPC-KT) derived from nasopharyngeal carcinoma. B95-8 virus can transform HUCLs but cannot superinfect Raji cells. P3HR-1 virus can transform HUCLs cells but cannot transform HUCLs. NPC-KT virus can transform HUCLs and can superinfect Raji cells. We have examined the time sequence of EBNA appearance and EA induction in HUCLs, BJAB cells and Ramos cells, in order to determine if three different strains of EBV differ in their abilities to infect their cells. We found that all three strains of EBV can induce EBNA in HUCLs, BJAB cells and Ramos cells. On the other hand, we found that P3HR-1 virus and NPC-KT virus can induce EA in BJAB cells and Ramos cells, but B95-8 virus cannot induce EA in their cells.

Antigens, Viral↗
PubMed1986

Rescue of a biologically active Epstein-Barr virus from nonproducer cells.

We recently established an epithelial/hybrid cell line, A2L/AH, by fusion of 8-azaguanine-resistant epithelial cells, Ad-AH, with a nonproducer lymphoblastoid cell line, A2L, using lymphocytes derived from the human nasopharynx transformed with the B95-8 strain of Epstein-Barr virus. The treatment of the parental A2L lymphoid cells with iododeoxyuridine led to the expression of Epstein-Barr virus early antigen, but neither virus capsid antigen or induction of Epstein-Barr virus DNA synthesis was observed. However, the treatment of the A2L/AH hybrid cells with iododeoxyuridine led to early antigen, virus capsid antigen and virus DNA synthesis, and the formation of virus particles. The virus rescued from the A2L/AH hybrid cells transforms human cord blood lymphocytes but is not able to induce early antigen in superinfected Raji cells.

Antigens, Viral↗
PubMed1986

Superinfection of epithelial hybrid cells (D98/HR-1, NPC-KT, and A2L/AH) with Epstein-Barr virus and the relationship to the C3d receptor.

Three Epstein-Barr virus (EBV) genome-positive epithelial/hybrid cell lines (D98/HR-1, NPC-KT, and A2L/AH) were superinfected with EBV derived from P3HR-1 (HR-1), NPC-KT, and B95-8 cells. The HR-1 virus is lytic and induces early antigen in superinfected Raji cells; the virus is not capable of transforming B-lymphocytes. Virus preparations from NPC-KT cells have both transforming and early antigen-inducing properties, while B95-8 virus can only transform B-lymphocytes. It was possible to demonstrate EBV antigens after superinfection of D98/HR-1 cells with both HR-1 virus and NPC-EBV. The NPC-KT hybrid cells, which were originally prepared by fusing human adenoid epithelial cells (Ad-AH) and EBV genome-positive NPC explanted epithelial cells, were susceptible to superinfection with HR-1 virus but not to NPC-EBV. The A2L/AH hybrid cells, which were prepared by fusion between Ad-AH cells and lymphocytes transformed by B95-8 virus, could not be superinfected with any of the virus preparations. In order to further investigate the nature of the EBV receptor as it relates to other cell membrane components, we examined cell surface markers on Ad-AH, NPC-KT, A2L/AH, and D98/HR-1 cells using monoclonal antibodies and by rosette formation. We found that the NPC-KT, A2L/AH, and Ad-AH cell lines express the OKB2 antigen and that the common acute lymphoblastic leukemia antigen is expressed on the A2L/AH cells. We also found that NPC-KT parental cells and a clone of NPC-KT cells express erythrocyte antibody complement b and erythrocyte antibody complement d, as determined by rosette formation, but were negative for C3b and C3d when monoclonal antibodies against these two markers were used. The D98/HR-1 cells were also confirmed to be negative for C3b and C3d. The data suggest that the C3d receptor may be part of the EBV receptor but that the C3d receptor, by itself, is not the only receptor to which EBV can bind.

Antibodies, Monoclonal↗