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T Ariga

Publications and source records attributed to T Ariga.

At least 109 records · Page 6Linked to original sources
PubMed1995

Regulation of glycolipid synthesis in HL-60 cells by antisense oligodeoxynucleotides to glycosyltransferase sequences: effect on cellular differentiation.

Treatment of the human promyelocytic leukemia cell line HL-60 with antisense oligodeoxynucleotides to UDP-N-acetylgalactosamine:beta-1,4-N-acetylgalactosaminyl-transferase (GM2-synthase; EC 2.4.1.92) and CMP-sialic acid:alpha-2,8-sialyltransferase (GD3-synthase; EC 2.4.99.8) sequences effectively down-regulated the synthesis of more complex gangliosides in the ganglioside synthetic pathways after GM3, resulting in a remarkable increase in endogenous GM3 with concomitant decreases in more complex gangliosides. The treated cells underwent monocytic differentiation as judged by morphological changes, adherent ability, and nitroblue tetrazolium staining. These data provide evidence that the increased endogenous ganglioside GM3 may play an important role in regulating cellular differentiation and that the antisense DNA technique proves to be a powerful tool in manipulating glycolipid synthesis in the cell.

Base Sequence↗
PubMed1995

Interleukin 1 beta up-regulates the expression of sulfoglucuronosyl paragloboside, a ligand for L-selectin, in brain microvascular endothelial cells.

Treatment of cultured bovine brain microvascular endothelial cells (BMECs) with interleukin 1 beta (IL-1 beta), an inflammatory cytokine, was shown to induce the accumulation of sulfoglucuronosyl paragloboside (SGPG), a glycolipid bearing the HNK-1 epitope. This resulted in the attachment of a greater number of human lymphocytes to the treated than to the untreated BMEC monolayers. Attachment of human lymphocytes to the IL-1 beta-activated BMEC cells could be blocked either by incubation of the human lymphocytes with an anti-L-selectin antibody or by application of an anti-SGPG antibody to the BMECs. These results suggest that SGPG may act as an important ligand for L-selectin for the regulation of the attachment of activated lymphocytes and their subsequent invasion into the nervous system parenchyma in inflammatory disorders of the central and peripheral nervous systems.

Animals↗
PubMed1995

Accumulation of isogloboside and ganglio-N-tetraosyl ceramide having blood group B determinant in the hepatomas of female LEC rats.

We have studied the neutral glycolipid composition of spontaneous hepatomas in LEC female rats. Neutral lipid fractions were isolated and purified by column chromatographies on DEAE-Toyopearl 650(M) and Iatrobeads. The neutral glycolipid fraction contained 3.2 to 4.4 micrograms lipid-bound glucose (Glc) per mg protein, and consisted of isogloboside (iso-Gb4, 50.8% of total neutral glycolipids) and IV3Gal, IV2Fuc, GgOse4Cer (asialo-BGM1, 13.5%) as the major neutral glycolipids and Gb3 and iso-Gb3 (9.2%), GlcCer (7.2%), LacCer (6.1%) as the other species. The structure of iso-Gb4 was elucidated by gas-liquid chromatography (GLC), permethylation study, liquid secondary ion (LSI) mass spectrometry, and nuclear Overhauser enhancement spectroscopy (NOESY) and that for asialo-BGM1 by GLC, LSI mass spectrometry, and high-performance thin-layer chromatography (HPTLC)-overlay method using anti-asialo-BGM1 antibody. Isogloboside and asialo-BGM1 which are found in negligible amounts in normal liver tissues may represent excellent markers for studying tumor metastasis and cellular adhesion.

ABO Blood-Group System↗
PubMed1995

A 15-base pair (bp) palindromic insertion associated with a 3-bp deletion in exon 10 of the gp91-phox gene, detected in two patients with X-linked chronic granulomatous disease.

Molecular genetic studies were carried out on two maternal cousins with X-linked chronic granulomatous disease (X-CGD). Sequencing analysis of polymerase chain reaction (PCR)-amplified DNA fragments from both patients revealed a 15-base pair (bp) insertion associated with a 3-bp deletion in exon 10 of the cytochrome b heavy chain (gp91-phox) gene. Results of genomic PCR with primers flanking the insertion/deletion site confirmed the mutation, and also demonstrated that their mothers were carriers for the disease. Palindromic sequences were found in the 15-bp insertion as well as in the flanking 3-bp deletion site, which may play a role in the mechanism of this mutation.

Adolescent↗
PubMed1995

Effect of nerve growth factor and forskolin on glycosyltransferase activities and expression of a globo-series glycosphingolipid in PC12D pheochromocytoma cells.

The glycosphingolipid (GSL) composition of cells changes dramatically during cellular differentiation. Nerve growth factor (NGF) or forskolin (FRK) are known to induce cellular differentiation including process formation in PC12 pheochromocytoma cells. In this respect, we present the NGF/FRK-dependent regulation of glycosyltransferase activities and the corresponding GSL expression in PC12D cells. After treatment of PC12D cells with NGF or FRK, the cell processes, including varicoses and growth cones, became strongly immunoreactive with an antibody against a unique globo-series neutral GSL, Gal alpha 1-3Gal alpha 1-4Gal beta 1-4Glc beta 1-1'Cer (GalGb3), and the activity of GalGb3-synthase increased significantly. Other glycosyltransferase activities, including GM1 containing blood group B determinant (BGM1)-, GM3-, GD1a-, and GM2-synthases, also increased significantly upon NGF treatment, but the immunoreactivity against BGM1 did not show any appreciable change. For the parent PC12 cells, NGF/FRK treatment significantly increased the percentage of anti-GalGb3 positive cells and induced some immunoreactive cell processes. Because the parent PC12 cells do not express appreciable amounts of GalGb3, and because PC12D cells are considered to be more differentiated than the parent PC12 cells, the expression of GalGb3 and the increase of GalGb3-synthase activity may be closely related to the cellular differentiation process in this cell line.

Animals↗
PubMed1995

[Establishment of superoxide production assay system using Epstein-Barr virus transformed cell line with chemiluminescence].

We established the system to detect superoxide produced by Epstein Barr virus lymphoblastoid cell line (EB-LCL). Superoxide production of EB-LCL was evaluated by measuring chemiluminescence (CL) enhanced with addition of horseradish peroxidase (HRP). Using this system, we measured CL of EB-LCL established from 13 patients with chronic granulomatous disease (CGD) and 8 normal individuals. Significant elevation of CL was observed in all control EB-LCLs, however, no remarkable CL was seen in any patients' EB-LCLs. We examined the effect of recombinant human interferon gamma (rh-IFN-gamma) and granulocyte colony stimulating factor (G-CSF) on CL of EB-LCL in vitro. With addition of rh-IFN-gamma, CL of normal control EB-LCL was significantly enhanced (p < 0.05), on the other hand, G-CSF was shown to have no effect. No significant CL was observed in any CGD patients' EB-LCLs even with addition of rh-IFN-gamma or G-CSF. It was suggested that superoxide produced by EB-LCL detected in this system was dependent on the same NADPH oxidase system which presents in phagocyte.

B-Lymphocytes↗
PubMed1995

[Experience in intra-hepatic-arterial chemotherapy and hepatic resection for metastatic colorectal cancer].

Out of 213 consecutive cases of colorectal cancer patients, 39 patients had liver metastasis (31 synchronous metastases and 8 metachronous metastases). One-and 3-year survivals of these patients with liver metastases were 46.5% and 30.1%, respectively. Twenty-four patients who were treated with intra-hepatic-arterial chemotherapy had better survival rates of 54.7% at 1 year, and 36.5% at 3 years than non-treated patients. Fifteen patients who underwent curative hepatic resection had better survival rates of 83.1% at 1 year, and 48.5% at 3 years than non-resected patients. Thirteen patients who underwent curative hepatic resection followed by intra-hepatic-arterial chemotherapy had good survival rates of 80.8% at 1 year, and 53.9% at 3 years. Seven patients who had multiple metastases to both lobes, were treated with intra-hepatic-arterial chemotherapy. These patients had a better survival rate of 22.9% at 1 year than non-treated patients.

Adenocarcinoma↗
PubMed1994

Glycolipid composition of human cataractous lenses. Characterization of Lewisx glycolipids.

We have studied the glycolipid composition of human cataractous lenses. Neutral and acidic lipid fractions were isolated by column chromatographies on DEAE-Sephadex and Iatrobeads. The neutral glycolipid fraction and acidic glycolipid fraction contained 0.6-0.9 micrograms of lipid-bound glucose (Glc) per mg of protein and 0.8-1.3 micrograms of lipid-bound sialic acid (NeuAc) per mg of protein, respectively. The neutral glycolipid fraction was found to contain LacCer (39.0% of total neutral glycolipids), Gb3 (16.2%), Gb4 (1.1%), nLc4 (5.0%), X (29.0%), and Y (9.2%). The acidic lipid fraction was found to contain mainly GM3 (33.1% of the total ganglioside fraction), GM1 (8.3%), LM1 (7.3%), GD1a (16.0%), and G (30.1%). The structures of neutral glycolipids X and Y and ganglioside G were elucidated by high performance thin-layer chromatography overlay method of glycolipids, gas-liquid chromatography, proton NMR spectrometry, and liquid secondary ion mass spectrometry as follows: 1) X, Gal beta 1-4(Fuc alpha 1-3)GlcNAc beta 1-3Gal beta 1-4Glc beta 1-1'Cer, III3FucnLc4 (Lex); 2) Y, Gal beta 1-4(Fuc alpha 1-3)GlcNAc beta 1-3Gal beta 1-4(Fuc alpha 1- 3)GlcNAc beta 1-3Gal beta 1-4Glc beta 1-1'Cer, V3FucIII3FucnLc6; and 3) G, NeuAc alpha 2-3Gal beta 1-4(Fuc alpha 1-3)GlcNAc beta 1-3 Gal-beta 1-4Glc beta 1-1'Cer, IV3NeuAcIII3FucnLc4 (sialosyl-Le(x)). A minor neutral glycolipid Z was isolated and tentatively characterized as GlcNAc beta 1-3?Gal beta 1-4(Fuc alpha 1-3)GlcNAc beta 1-3Gal beta 1-4Glc beta 1-1'Cer (GlcNAc-Le(x)), suggesting that it may be the precursor of glycolipid Y. The major long-chain base of these human cataract glycolipids was C18:0 sphingosine (sphinganine). The major fatty acids were C16:0, C24:1 and C24:0, and monounsaturated fatty acids accounted for 40-55% of the total fatty acids.

Aged↗
PubMed1994

Generation of one set of murine monoclonal antibodies specific for globo-series glycolipids: evidence for differential distribution of the glycolipids in rat small intestine.

We generated four murine monoclonal antibodies (MAbs) specific for globo-series glycolipids by immunizing C3H/HeN mice with these purified glycolipids adsorbed to Salmonella minnesota followed by fusion with mouse myeloma cells. By use of a wide variety of glycolipids, the precise structures recognized by these MAbs were elucidated through an enzyme-linked immunosorbent assay and an immunostaining on thin-layer chromatography. These four MAbs, designated as BGR23, BGR47, BMR26, and BGR27, exhibited highly restricted binding specificities, reacting only with the globo-series glycolipids Gb3Cer, III3Gal alpha-Gb3Cer, Gb4Cer, and IV3GalNAc alpha-Gb4Cer, respectively, which were used for immunization. None of the other various glycolipids or gangliosides were recognized. We determined the localization of these globo-series glycolipids in adult rat small intestine by means of an immunofluorescence technique with these MAbs. Our study revealed that there is a differential distribution of these glycolipids in the rat tissue. III3Gal alpha-Gb3Cer was demonstrated on the cryptic cells and circular muscle, whereas Gb4Cer was localized on both the circular and longitudinal muscles. The expression of Gb3Cer was associated with the epithelium and the capillary endothelial cells in the lamina propria mucosae as well as with the tunica submucosa, whereas IV3GalNAc alpha-Gb4Cer was detected on the epithelium, capillary endothelial cells in the lamina propria mucosae, and both the muscle layers.

Animals↗
PubMed1994

Glycosphingolipid antigens in cultured bovine brain microvascular endothelial cells: sulfoglucuronosyl paragloboside as a target of monoclonal IgM in demyelinative neuropathy [corrected].

Since a number of anti-glycosphingolipid (GSL) antibody activities have been demonstrated in patients with various neurological disorders, the presence of common antigens between brain microvascular endothelial cells (BMECs) and the nervous tissues presents a potential mechanism for the penetration of macromolecules from the circulation to the nervous system parenchyma. We first investigated GSL composition of cultured bovine BMECs. Bovine BMECs express GM3(NeuAc) and GM3(NeuGc) as the major gangliosides, and GM1, GD1a, GD1b, GT1b, as well as sialyl paragloboside and sialyl lactosaminylparagloboside as the minor species. Sulfoglucuronosyl paragloboside was also found to be a component of the BMEC acidic GSL fraction, but its concentration was lower in older cultures. On the other hand, the amounts of neutral GSLs were extremely low, consisting primarily of glucosylceramide. In addition, we analyzed the effect of anti-SGPG IgM antibody obtained from a patient of demyelinative polyneuropathy with macroglobulinemia against cultured BMECs. Permeability studies utilizing cocultured BMEC monolayers and rat astrocytes revealed that the antibody facilitated the leakage of [carboxy-14C]-inulin and 125I-labeled human IgM through BMEC monolayers. A direct cytotoxicity of this antibody against BMECs was also shown by a leakage study using [51Cr]-incorporated BMECs. This cytotoxicity depended on the concentration of the IgM antibody, and was almost completely blocked by preincubation with the pure antigen, sulfoglucuronosyl paragloboside. Our present study strongly supports the concept that immunological insults against BMECs induce the destruction or malfunction of the blood-nerve barrier, resulting in the penetration of the immunoglobulin molecule to attach peripheral nerve parenchyma.

Animals↗
PubMed1994

Molecular genetic studies of two families with X-linked chronic granulomatous disease: mutation analysis and definitive determination of carrier status in patients' sisters.

Molecular genetic studies of two families with X-linked chronic granulomatous disease (X-CGD) were performed. The patients showed abnormal patterns on Southern blot analysis using cytochrome b heavy chain (CYBB) cDNA as a probe. Both patterns differed and neither has ever been observed in normal individuals. We applied the results to the diagnosis of the carrier state in the patients' sisters. The results clearly demonstrated that each patient's sister possessed the same abnormal allele as the patient's CYBB gene, as detected by Southern analysis. Thus, the results confirm that both of the patients' sisters are carriers of the disease. Further molecular analysis of the patients' mutation revealed that they were a point mutation, and a partial deletion of the CYBB gene, respectively. These mutations have not previously been reported.

Amino Acid Sequence↗
PubMed1994

Assignment of the human moesin gene (MSN) to chromosome region Xq11.2-->q12.

The human moesin gene (MSN) was mapped to the long arm of the X chromosome. PCR products for the moesin gene cDNA were used as probes to isolate their corresponding cosmid clones. Fluorescence in situ hybridization (FISH) with two of the isolated cosmid probes showed signals at Xq11.2-->q12, whereas four other cosmids showed FISH signals on chromosome 5. Southern blot hybridization, using a PCR product corresponding to the 3' region of the moesin gene cDNA as a probe (probe-3), on one of the two cosmids that produced signals on the X chromosome gave 5.7- and 3.5-kb HindIII fragments. Further Southern hybridization of the DNA from XY, XX, and XXXXX individuals using probe-3 revealed a gene-dose effect of the X chromosome on the size of a 3.5-kb and a 3.0-kb HindIII fragment; in contrast, an invariant 9.8-kb band was present in the DNA of all individuals tested. Sequencing of an exon-intron border revealed that the two cosmids had predicted sequences. These results indicated that the two cosmids contained MSN, and it was consequently assigned to human chromosome region Xq11.2-->q12. These results strongly suggest that MSN may be removed from candidacy for Wiskott-Aldrich syndrome, which has been putatively mapped to Xp11.3-->p11.22.

Chromosome Mapping↗