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S Yui

Publications and source records attributed to S Yui.

At least 37 records · Page 2Linked to original sources
PubMed1993

Characterization of cell growth-inhibitory factor in inflammatory peritoneal exudate cells of rats.

We characterized the nature and reaction mode of the cell growth-inhibitory factor (here designated CGIF) from rat peritoneal exudate cells (PEC). The soluble fraction separated from the lysate of Enterococcus faecalis-induced 24 hr PEC completely inhibited Con A-induced thymocyte mitogenesis. Gel filtration chromatography showed that CGIF has a molecular weight of approximately 23-25 kDa. Isoelectric focusing with Rotofor indicates that the factor has an isoelectronic point of 5.8-6.4. CGIF was inactivated by treatment at 70 C, for 30 min or by tryptic digestion, but the activity was not destroyed by the reduction with dithiothreitol. As well as thymocyte proliferation, CGIF completely suppressed 3H-thymidine incorporation of splenocytes which were stimulated by either Con A or LPS, suggesting the factor is effective on both T and B cells. The acting point of the inhibitor appeared to be a later stage of the lymphocyte activation sequence, since it was still effective when added 28.5 hr after the addition of Con A. CGIF also reduced the viability of these cells when added with mitogens such as Con A or LPS. CGIF thus appears to be distinct from interleukin-1 receptor antagonist or transforming growth factor-beta.

Animals↗
PubMed1993

Induction of murine macrophage growth by modified LDLs.

We previously reported that cell membrane components and lipoproteins were able to induce the growth of murine peritoneal macrophages. The aim of the present study was to examine whether macrophage growth could also be induced by chemically modified lipoproteins, such as acetylated low density lipoprotein (acetyl-LDL) or oxidized LDL, ligands known to be endocytosed by the macrophage scavenger receptors. When murine peritoneal exudate macrophages were cultured in vitro with 25-100 micrograms/mL acetyl-LDL or oxidized LDL, significant growth was induced. On comparing the dose-response curves of these LDLs, a more potent effect was seen with oxidized LDL than acetyl-LDL, especially on resident macrophages. On the other hand, growth of these cells was not stimulated by native (unmodified) LDL or high density lipoprotein. These in vitro data revealed a new function of chemically modified LDLs as effective inducers of macrophage cell growth. This aspect may be physiologically relevant to the growth of macrophage foam cells in situ in the development of atherosclerosis.

Animals↗
PubMed1993

Heat stable interleukin-1 activity and activity inhibiting thymocyte proliferation in inflammatory polymorphonuclear leukocytes.

The present study demonstrates the co-existence of heat stable interleukin-1 (IL-1) and IL-1-suppressing activity in murine inflammatory polymorphonuclear leukocytes (PMNs). When the IL-1 activity in casein-induced PMN lysate was examined by lymphocyte activating factor assay, it peaked at a concentration of 2.5 x 10(6) cells per ml, but this activity was reduced to nothing at higher concentrations, suggesting the co-existence of IL-1 and IL-1-suppressive factors in PMNs. Although IL-1 has been reported to be inactivated by heat treatment, approximately one-fourth of the IL-1 activity was restored after treatment at 100 degrees C for 10 min. In gel chromatography, the IL-1 activity of the PMN-soluble fraction was eluted in two broad peaks with apparent molecular sizes of 17-23 kDa and 23-43 kDa, respectively. Since the heat stable IL-1 activity was mainly eluted in fractions corresponding to the latter peak, and was neutralized by IL-1 receptor antagonist (IL-1ra) or anti-IL-1 alpha antiserum, the heat stable IL-1 is suggested to be precursor form IL-1 alpha. A high concentration of soluble fraction from PMN lysate, in contrast, completely suppressed the activity of recombinant IL-1 alpha or beta, and the suppressive activity was heat labile. Since thymocyte mitogenesis by 5 micrograms/ml of concanavalin A (Con A) with or without IL-2 was also completely suppressed, the suppressive factor(s) may not be IL-1ra or transforming growth factor beta which were reported to be present in PMNs.

Animals↗
PubMed1991

Augmentation and suppression of release of tumor necrosis factor from macrophages by negatively charged phospholipids.

We recently reported that some lipid species of cell membranes and lipoproteins induced the growth of peripheral macrophages. In this study, the effects of phospholipids on tumor necrosis factor (TNF)-releasing activity of macrophages were examined. Ten to 20 micrograms/ml of cardiolipin, which is a suboptimal concentration for macrophage growth-stimulation, augmented macrophage TNF release triggered by lipopolysaccharide (LPS) in vitro. This priming effect appeared with 1 day of preincubation and was still potent on day 3, whereas the priming effect of interferon-gamma (IFN-gamma) peaked at 3 h and then gradually decreased. In contrast, a high concentration of cardiolipin (40 micrograms/ml) which is optimal for the induction of macrophage growth, completely suppressed LPS-triggered TNF release from not only untreated macrophages but also IFN-gamma-primed macrophages. The suppressive effect was potent even with 3 h preincubation, was still potent on day 3, and was not abolished by indomethacin. Cardiolipin had scarcely any effect on the triggering activity of LPS. Similar augmentative and suppressive activities were observed in peroxidized phosphatidylserine, which is also highly active in inducing macrophage growth, but was not found in native phosphatidylserine, which is less active in inducing macrophage growth, but was not found in native phosphatidylserine, which is less active, nor in phosphatidylcholine, which is an inactive species toward macrophage growth. These results suggest that lipids may be important endogenous factors in regulating both activation and growth states of peripheral macrophages.

Animals↗
PubMed1990

Comparative studies on lipid and colony-stimulating factor-induced macrophage growth.

We previously reported that lipids such as cholesterol esters, triglycerides, and some phospholipids that constitute cell membranes or serum lipoproteins induced growth of mouse peritoneal macrophages in vitro. In this paper, we compared the macrophage growth-stimulating activity of cardiolipin (CL), an active phospholipid with that of CSF-1. Growth kinetics and maximal degree of growth of exudated macrophages induced by CL were similar to those of CSF-1. CL did not stimulate macrophages to release soluble macrophage growth factors. Also, the activity of CL was not blocked as much by anti-CSF-1, suggesting that most of the effect of CL was direct and not mediated by CSF-1 or other protein factors. There was no synergistic effect between CL and CSF-1. CL induced growth of both exudate and resident macrophages, whereas CSF-1 induced very little resident macrophage growth. Furthermore, although the growth-stimulating activities of both substances were inhibited by IFN-gamma and TNF, CL was more resistant to these inhibitory effects. These results suggest that the lipid has some different characters from CSF-1 and may induce the growth of resident macrophages in inflammations or tumors.

Animals↗
PubMed1990

Augmentation of macrophage growth-stimulating activity of lipids by their peroxidation.

Previously, we reported that some kinds of lipids (cholesterol esters, triglycerides, and some negatively charged phospholipids) that are constituents of lipoproteins or cell membranes induce growth of peripheral macrophages in vitro. In this paper, we examined the effect of peroxidation of lipids on their macrophage growth-stimulating activity because lipid peroxidation is observed in many pathological states such as inflammation. When phosphatidylserine, one of the phospholipids with growth-stimulating activity, was peroxidized by UV irradiation, its macrophage growth-stimulating activity was augmented in proportion to the extent of its peroxidation. The activity of phosphatidylethanolamine was also increased by UV irradiation. On the other hand, phosphatidylcholine or highly unsaturated free fatty acids, such as arachidonic acid and eicosapentaenoic acid, did not induce macrophage growth irrespective of whether they were peroxidized. The augmented activity of UV-irradiated phosphatidylserine was not affected by the coexistence of an antioxidant, vitamin E or BHT. These results suggest that some phospholipids included in damaged cells or denatured lipoproteins which are scavenged by macrophages in vivo may induce growth of peripheral macrophages more effectively when they are peroxidized by local pathological processes.

Animals↗
PubMed1989

Neutral lipid accumulation in macrophages during lipid-induced macrophage growth.

We previously reported that lipids such as cholesterol esters, triglycerides, and some phospholipids that are components of cell membranes or serum lipoproteins induced the growth of mouse peritoneal macrophages in vitro. Here, we report that macrophage growth was directly induced by lipids without any soluble factors and that the continuous presence of lipids was required for their growth during culture. When macrophages were cultured with several phospholipids that stimulated macrophage growth, their triglyceride content was dramatically increased during culture, whereas their contents of phospholipids, cholesterol, and esterified cholesterols were scarcely changed. On the other hand, phosphatidylcholine and sphingomyelin, which did not stimulate macrophage growth, caused less accumulation of triglycerides in the cells. Macrophages in which triglycerides accumulated resembled foam cells, since they contained many particles that stained with oil red O. Macrophages that cultured with cholesteryl linoleate also contained many oil red O-stainable particles. These data suggest that accumulation of lipid droplets is correlated with macrophage growth induced by lipids and that foam cells in pathological states such as those in atherosclerotic or xanthoma lesions might proliferate in situ.

Animals↗
PubMed1988

Mucinous colorectal carcinoma: clinical pathology and prognosis.

Mucinous carcinomas accounted for 37 (6.4%) of 540 cases of colorectal carcinoma. The clinical and pathological features of these mucinous carcinomas were compared with those of the 510 well or moderately differentiated adenocarcinomas. Mucinous carcinoma was more common in the patients 39 years of age or under (P less than 0.05) and was more frequent in the female patients. A large number of mucinous carcinomas were located in the rectum, followed by the right colon. However, the right colon showed a higher relative incidence (40.5% vs 12.5%, P less than 0.005). Mucinous carcinoma was characterized by infiltration of the surrounding tissues (24.3% vs 7.8%, P less than 0.005), positive lymph node involvement (75.7% vs 48.6%, P less than 0.005), and peritoneal implant (21.6% vs 4.1%, P less than 0.005). The cumulative five and ten year survival rates after resection of mucinous carcinoma were 45.5 per cent and 39.8 per cent, respectively, and those after curative resection, 72.4 per cent and 63.5 per cent, respectively. These survival rates were lower, without significant differences, than those for the well or moderately differentiated adenocarcinomas. The results suggest the need for aggressive lymph node dissection and wide excision of the surrounding tissues for mucinous carcinoma, with special attention paid to local recurrence.

Adenocarcinoma↗
PubMed1987

Assay of glycosidase by lectin affinity high-performance liquid chromatography.

Human transferrin was incubated with sialidase and beta-galactosidase and then examined by lectin affinity high-performance liquid chromatography (HPLC). The elution patterns were changed according to the period of incubation and the amount of enzyme. This method of studying lectin affinity HPLC using human transferrin as a substrate makes possible the rapid and important detection of glycosidase activity.

Chromatography, High Pressure Liquid↗
PubMed1987

Systematic fractionation of oligosaccharides of human immunoglobulin G by serial affinity chromatography on immobilized lectin columns.

Human immunoglobulin G is known to contain 16 different biantennary complex-type asparagine-linked sugar chains, each of which occurs in a nonsialylated, monosialylated, or disialylated form. These oligosaccharides can be separated into 14 fractions by sequential affinity chromatography with Aleuria aurantia lectin (AAL)-Sepharose, RCA120-WG003, and E4-phytohemagglutinin-agarose columns. Twelve of them were found to contain a single oligosaccharide, while the fraction which passed through all three columns was shown to contain two oligosaccharides, GlcNAc beta 1----2Man alpha 1----6(+/- GlcNAc beta 1----4) (GlcNAc beta 1----2Man alpha 1----3)Man beta 1----4GlcNAc beta 1----4GlcNAcOT. The fraction, which bound to the AAL-Sepharose column and passed through the remaining two lectin columns, also contained two oligosaccharides, GlcNAc beta 1----2Man alpha 1----6(+/- GlcNAc beta 1----4) (GlcNAc beta 1----2Man alpha 1----3)Man beta 1----4GlcNAc beta 1----4 (Fuc alpha 1----6)GlcNAcOT. These results indicated that serial affinity chromatography with the three lectin columns can be used effectively to detect changes in the sugar chains of IgG resulting from diseases such as rheumatoid arthritis.

Arthritis, Rheumatoid↗
PubMed1987

Relationship of ability of phospholipids to stimulate growth and bind to macrophages.

Among the phospholipids normally present in mammalian cell membranes, the negatively charged phospholipids, phosphatidylserine (PS), phosphatidylglycerol, and cardiolipin, and the neutral phospholipid phosphatidylethanolamine--but not phosphatidylcholine (PC) or sphingomyelin--were found to induce growth of peripheral macrophages. By use of liposomes prepared from PS, which stimulated growth, and PC, which did not, the relation between growth-stimulating activity and binding of the phospholipids to macrophages was studied. The growth-stimulating activity of PS/PC liposomes decreased with increase in their relative content of PC. The amount of PS bound to macrophages also decreased with increase in the proportion of PC in PS/PC liposomes. These decreases in growth-stimulating and binding activities were both partly recovered by additional incorporation into the PS/PC liposomes of cholesterol, which is also a cell membrane component. Phospholipids that stimulated macrophage growth showed high binding ability to macrophages, whereas those that did not stimulate growth scarcely bound to macrophages. Thus the macrophage growth-stimulating activities of phospholipids correlated well with their ability to bind to macrophages. These liposome models should be useful in elucidating the early mechanism of induction of macrophage growth by lipid materials such as cell debris and lipoproteins.

Animals↗
PubMed1986

Cross-linking between 16S ribosomal RNA and protein S4 in Escherichia coli ribosomal 30S subunits effected by treatment with bisulfite/hydrazine and bromopyruvate.

Cytosine in nucleic acids can be modified by treatment with a mixture of bisulfite and hydrazine. The reaction is specific for single-stranded regions of nucleic acids and the product is N4-aminocytosine. Bromopyruvate has been used for alkylation of protein SH groups and through its 2-oxo group it can form a hydrazone with N4-aminocytosine. Escherichia coli ribosomal 30S subunits were treated with 1 M sodium bisulfite + 2 M hydrazine in the presence of 10 mM MgCl2 at pH 7.0 and 37 degrees C for 30 min. By this treatment, 2.4 cytosine residues/molecule 16S rRNA were derivatized into N4-aminocytosines. 35S-labeled 30S subunits were modified in this way and then treated with 10 mM bromopyruvate at pH 8.0 and 37 degrees C for 5 min. Analysis in sodium dodecyl sulfate/sucrose density gradient centrifugation showed co-sedimentation of a part of the 35S radioactivity with the RNA. The co-sedimentation was dependent on both the bisulfite/hydrazine and the bromopyruvate treatments. The RNA-protein complex was prepared from unlabeled 30S subunits. The protein portion was labeled with 125I, the RNA portion was digested with nucleases, and then the hydrazone linkage between the protein and oligonucleotides was cleaved by treatment with 0.2 M HCl. The oligonucleotides formed were removed by dialysis and the protein was identified as S4 by two-dimensional electrophoresis and by sodium dodecyl sulfate/polyacrylamide gel electrophoresis. The results indicate that the cysteinyl residue of protein S4 at position 31 from the N-terminus is located close to a cytosine residue which is non-base-paired and easily accessible by the externally present bisulfite/hydrazine reagent.

Electrophoresis, Polyacrylamide Gel↗
PubMed1986

Induction of macrophage growth by lipids.

Lipoproteins from ascitic tumors in mice and lipids extracted from these lipoproteins induced growth of murine peritoneal macrophages in vitro. The lipid components with activity were examined by use of lipid vesicles or liposomes. Liposomes prepared from egg-yolk PC alone did not induce macrophage growth, but those prepared from mixtures of egg-yolk PC and cholesterol or cholesteryl esters other than cholesteryl oleate, or triglycerides other than triolein, enhanced 3H-TdR incorporation into macrophages. The free fatty acids examined had no effect on 3H-TdR incorporation. These results suggest that growth of macrophages is induced by ordinary lipids present in lipoproteins or cell membranes that the macrophages scavenge in the body.

Animals↗
PubMed1986

Induction of macrophage growth by effete cells.

When mouse peritoneal cells in early phase-inflammatory exudates were cultured in vitro, the number of polymorphonuclear leukocytes (PMNs) rapidly decreased, whereas the number of macrophages gradually increased during culture. Macrophage growth was also induced by addition of effete PMNs or their debris to macrophage monolayers. This phenomenon was not restricted to senescent PMNs, because effete spleen cells or effete tumor cells also induced macrophage growth. The activity of these cell debris was stable on heating at 100 degrees C and was partially recovered in the lipid fraction. These data suggest that tissue macrophages may proliferate when they scavenge effete PMNs or other host cells and that these cell debris may be important mediators in inducing growth of peripheral macrophages in inflammation and tumors or the normal steady state.

Animals↗
PubMed1986

Induction of macrophage growth by negatively charged phospholipids.

The effects on macrophage growth of seven phospholipids that are normally present in cell membranes were examined. Phosphatidylcholine and sphingomyelin which are the main phospholipid constituents of mammalian cell membranes, had no effect on growth of macrophages. Phosphatidylinositol also had little effect. On the other hand, the relatively minor components phosphatidylserine, phosphatidylglycerol, cardiolipin, and phosphatidic acid, which are negatively charged phospholipids, significantly enhanced macrophage growth. These findings suggest that some acidic phospholipids may increase survival or growth of tissue macrophages when they are ingested by the cells in materials containing phospholipids, such as effete autologous cells or bacteria.

Animals↗
PubMed1985

Induction of macrophage growth by the lipid moiety of lipoprotein and its augmentation by denaturation of the lipoproteins.

Lipoprotein (d less than 1.21) isolated from mouse tumor ascitic fluid or mouse-serum induced growth of peritoneal macrophages in vitro. Lipoprotein fractions that stimulated macrophage growth were the chylomicron, very-low-density lipoprotein (VLDL), and low-density lipoprotein (LDL), whereas the high-density lipoprotein (HDL) fraction did not. Lipids extracted from total lipoprotein also showed significant macrophage-growth-stimulating activity and lost this activity when hydrolyzed. The macrophage-growth-stimulating activity of the lipoprotein (d less than 1.21) was increased about ten times by heat treatment of the lipoprotein (100 degrees C, 30 min). The HDL fraction that had no activity in the native form also showed activity after heat treatment. Lipoprotein-depleted ascitic fluid and simple proteins such as bovine serum albumin (BSA) had no activity even after heat treatment. These results show that the lipid moiety of lipoproteins caused proliferation of macrophages and that denatured lipoproteins were more effective than native ones.

Animals↗