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J Masuyama

Publications and source records attributed to J Masuyama.

At least 19 recordsLinked to original sources
PubMed2001

The molecular mechanisms of post-adhesive transmigration of T cells.

Leukocyte extravasation is an essential phenomenon in inflammatory responses of the body. However, less is known about the mechanisms of transendothelial migration of leukocytes subsequent to their adhesion to the endothelium. It could be considered that at least three different cellular responses participate in the transmigration of adherent leukocytes: 1) polarization of adherent cells in cell shape, 2) interactions between adherent cells and molecules bound to the endothelial surface to stimulate migration through the junction between adjacent endothelial cells, and 3) co-ordination with endothelial cells to open the junction. Molecules involved in these events are discussed in this review.

Animals↗
PubMed2000

Nucleolin as the earliest target molecule of autoantibodies produced in MRL/lpr lupus-prone mice.

To elucidate the autoantigen against which autoantibodies are produced in the earliest phase of the disease process of systemic lupus erythematosus (SLE), serum samples were collected individually and serially from 10 NZB/NZW F1 and 10 MRL/lpr mice. Using immunoblots with mouse thymoma cell (EL-4) lysates as substrates, all mice were found to generate autoantibody against an either 150-kDa, 110-kDa, 75-kDa, or 55-kDa molecule in as early as 4 weeks. Anti-DNA antibodies occurred almost at the same time or after those against these four molecules. The number of antigens reactive with autoantibodies in immunoblots increased gradually with age. Antibodies against histone molecules were produced after 8 weeks of age. Among the four antigens, the 110-kDa molecule was identified as nucleolin, which is an abundant nucleolar phosphoprotein. Nucleolin binds DNA, RNA, and nucleic acid-binding proteins such as histone H1. Nucleolin is a target of granzyme A of cytotoxic T cells, and autoantibodies against it are found in sera from patients with SLE as well as from those with various viral infections. These results indicate that nucleolin is one of the immunodominant molecules that break down self-tolerance and initiate autoantibody-spreading in a mouse model of SLE.

Aging↗
PubMed2000

[Three patients with systemic sclerosis complicated by microangiopathic hemolytic anemia and thrombocytopenia].

Clinical profiles and the treatment process of three female patients with systemic sclerosis (cases 1, 2, and 3) complicated by thrombotic microangiopathic hemolytic anemia (TMHA) were described. Thrombocytopenia preceded renal damage and hypertension in cases 1 and 2, although the chronological relationship between these parameters were unknown in case 3. Plasma exchange therapy using fresh frozen plasma was beneficial in cases 1 and 2. Cases land 3 presented with delirium and fluctuating psychosis, respectively. Early detection of thrombocytopenia and insidious hemolysis might be essential for starting effective plasmapheresis treatment in a part of patients with scleroderma kidney who present with thrombotic thrombocytopenic purpura (TTP) like disorder.

Aged↗
PubMed1999

Characterization of the 4C8 antigen involved in transendothelial migration of CD26(hi) T cells after tight adhesion to human umbilical vein endothelial cell monolayers.

In extravasation of T cells, little is known about the mechanisms of transendothelial migration subsequent to the T cells' tight adhesion to endothelium. To investigate these mechanisms, we developed a monoclonal antibody (mAb), termed anti-4C8, that blocks transmigration but not adhesion in a culture system in which high CD26-expressing (CD26(hi)) T cells preferentially migrate through human umbilical vein endothelial cell (HUVEC) monolayers cultured on collagen gels. Anti-4C8 reacted with all CD3(+) T cells and monocytes but not neutrophils or HUVECs. The structure defined by this antibody was an 80-kD molecule. The mAb at 1 mug/ml inhibited 80-90% of migration of CD3(+) T cells through unstimulated and interferon gamma-stimulated HUVEC monolayers without interfering with adhesion and cell motility. When added to the cultures after the adhesion, anti-4C8 completely blocked subsequent transmigration of adherent T cells. Phase-contrast and electron microscopy revealed that T cells are arrested at the intercellular junctions of HUVECs in the presence of anti-4C8. Anti-4C8 exhibited agonistic effects on resting T cells without other stimuli under culture conditions in which anti-4C8 can stimulate T cells. First, in the checkerboard assay using collagen gels, the antibody promoted chemokinetic migration of the cells in a dose-dependent manner from 0.1 to 10 mug/ml. The predominant population of T cells that migrated into collagen gels with impregnated anti-4C8 were CD26(hi). Second, solid-phase-immobilized anti-4C8 induced adhesion of T cells to the substrate, often with polarizations in cell shape and large pseudopods rich in filamentous (F-) actin. Third, soluble anti-4C8 augmented F-actin content preferentially in CD26(hi) T cells when added to T cells at a high dose of 10 mug/ml. Finally, both anti-4C8-induced chemokinetic migration and transendothelial migration were inhibited by pretreatment of T cells with pertussis toxin. These findings suggest that stimulation via the 4C8 antigen increases cell motility of CD26(hi) cells with profound cytoskeletal changes through signaling pathways including G proteins. The 4C8 antigen may be involved in preferential transmigration of CD26(hi) cells adherent to HUVECs.

Actins↗
PubMed1999

Circulating myeloperoxidase and anti-myeloperoxidase antibody in patients with vasculitis.

To evaluate a role of myeloperoxidase (MPO) and antibody to myeloperoxidase (anti-MPO) in vasculitis, MPO and anti-MPO were determined by enzyme-linked immunosorbent assays in sera from 43 patients with vasculitis, 40 with rheumatoid arthritis, 36 with systemic lupus erythematosus (SLE), 23 with mixed connective tissue disease, 13 with systemic sclerosis, 22 with polymyositis/dermatomyositis, 18 with Sjögren's syndrome, and 30 normal controls. Kidney and lung sections from patients with vasculitis were stained for MPO. Anti-MPO titers were significantly higher (p<0.005) in the patients with vasculitis (mean+/- SD absorbance at 405 nm: 0.53 +/- 0.37) than in any other groups (0.15 +/- 0.04 to approximately 0.21 +/- 0.11). MPO levels in patients with vasculitis were comparable with those in patients with other diseases except SLE. In two patients with vasculitis, anti-MPO decreased sharply with simultaneous increases in MPO 1-2 weeks after they developed pulmonary hemorrhage. Numerous cells positive for MPO infiltrated the Bowman's spaces. These results indicate that MPO may contribute to the pathogenesis of vasculitis and a sudden fall in anti-MPO may predict a poor prognosis in some cases.

Animals↗
PubMed1999

UDP-GlcNAc:Galbeta1-->3GalNAc (GlcNAc to GalNAc) beta1-->6N-acetylglucosaminyltransferase holds a key role on the control of CD15s expression in human pre-B lymphoid cell lines.

Expression mechanism of CD15s (sialyl-Lex, sLex) antigen has been investigated using human B lymphoid cell lines. sLexstructures were not expressed in mature B lymphoids but highly expressed in pre-B leukemia and pre-B lymphoma cell lines. The expression site was mainly on the O -linked oligosaccharide chains and E-selectin mediated-cell adhesion capability of sLex-positive cells were significantly suppressed by benzyl-alpha-GalNAc treatment. Subsequently, the bases of the sLexexpression control mechanism were examined at the levels of enzymatic activities and transcripts of glycosyltransferases. (1) The activities of alpha1-->3fucosyltransferase, alpha2-->3sialyltransferase, beta1-->4Gal-transferase, and elongation beta1-->3GlcNAc-transferase, did not correlate with sLexexpression levels. (2) The transcripts of Fuc-TVII were not parallel with sLexexpression, and those of ST3Gal IV and beta1-->4Gal-transferase were constitutively detected in all cell lines tested. (3) There was no detectable enzyme activity for core 3 and 4 backbone structure synthesis in human B cell lines. (4) By contrast, the enzyme activities and transcripts of UDP-GlcNAc:Galbeta1-->3GalNAc (GlcNAc to GalNAc) beta1-->6 N -acetylglucosaminyltransferase (Core2GnT) had significant correlation with the cell surface expression of sLexantigen. (5) Moreover, Western blot analysis revealed the presence of a major approximately 150 kDa glycoprotein that carries O -linked oligosaccharides recognized by anti-sLexmonoclonal antibody in sLex-positive pre-B leukemia cell lines. This correlation of Core2GnT with CD15s expression suggests that Core2GnT is a regulator of the cell surface expression of sLexin human pre-B lymphoid cells.

Antigens, CD↗
PubMed1999

Probing the substrate specificity of the intracellular brain platelet-activating factor acetylhydrolase.

Platelet-activating factor acetylhydrolases (PAF-AHs) are unique PLA2s which hydrolyze the sn-2 ester linkage in PAF-like phospholipids with a marked preference for very short acyl chains, typically acetyl. The recent solution of the crystal structure of the alpha(1) catalytic subunit of isoform Ib of bovine brain intracellular PAF-AH at 1.7 A resolution paved the way for a detailed examination of the molecular basis of substrate specificity in this enzyme. The crystal structure suggests that the side chains of Thr103, Leu48 and Leu194 are involved in substrate recognition. Three single site mutants (L48A, T103S and L194A) were overexpressed and their structures were solved to 2.3 A resolution or better by X-ray diffraction methods. Enzyme kinetics showed that, compared with wild-type protein, all three mutants have higher relative activity against phospholipids with sn-2 acyl chains longer than an acetyl. However, for each of the mutants we observed an unexpected and substantial reduction in the V(max) of the reaction. These results are consistent with the model in which residues Leu48, Thr103 and Leu194 indeed contribute to substrate specificity and in addition suggest that the integrity of the specificity pocket is critical for the expression of full catalytic function, thus conferring very high substrate selectivity on the enzyme.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1998

Human monocyte-endothelial cell interaction induces platelet-derived growth factor expression.

OBJECTIVE: The purpose of this study was to investigate whether the synthesis of platelet-derived growth factor (PDGF), a major mitogen and chemoattractant for vascular smooth muscle cells, was induced by the direct cell-to-cell interaction between human monocytes and umbilical vein endothelial cells (ECs). METHODS: PDGF protein and mRNA expression were determined by cellular ELISA, immunohistochemical and Northern blot analyses. RESULTS: Coculture of monocytes and ECs secreted a large amount of PDGF into the supernatant, whereas culture of ECs or monocytes alone induced low levels of PDGF production. In Northern blot analysis, substantial amounts of PDGF-A and -B mRNA were induced by coculture of monocytes with ECs. Immunohistochemistry revealed that PDGF-B chain protein was detectable in both ECs and monocytes. PDGF production by ECs induced by conditioned medium of the coculture was significantly inhibited by Abs against interleukin-1 beta (IL-1 beta) and tumor necrosis factor- alpha (TNF alpha). CONCLUSIONS: These results indicate that the direct cell-to-cell interaction between human monocytes and ECs induces PDGF synthesis in both types of cells, suggesting that PDGF produced locally by monocyte-EC adhesive interaction plays an important role in the pathogenesis of atherosclerosis by promoting the migration and accumulation of vascular smooth muscle cells.

Antibodies, Monoclonal↗
PubMed1998

Acute acalculous cholecystitis in systemic lupus erythematosus: a case report and review of the literature.

A 27-year-old woman with systemic lupus erythematosus (SLE) was found to have acute acalculous cholecystitis. At the time of admission, the patient was not under corticosteroid or immunosuppressive therapy. Computed tomography (CT) and ultrasonography revealed findings in the gall bladder consistent with acute acalculous cholecystitis. Her abdominal pain completely disappeared following corticosteroid therapy, with dramatic improvement in the images of CT and ultrasonography. Six similar cases of SLE complicated with acute acalculous cholecystitis have been reported in the literature and they were all treated surgically by cholecystectomy or cholecystostomy. This is the first case report in which acute acalculous cholecystitis accompanying SLE was treated successfully by corticosteroid without surgical intervention.

Acute Disease↗
PubMed1997

Monocytes modulate the fibrinolytic balance of endothelial cells.

Cultured endothelial cells (ECs) produced a constitutive plasminogen activator inhibitor-I (PAI-1), whereas primary culture of monocytes from blood did not produce a detectable amount of PAI-1. Addition of monocytes to ECs caused the accumulation of a large amount of PAI-1 in the supernatant in a dose- and time-dependent manner. Having almost no effect on the production of tissue-type plasminogen activator (t-PA), monocytes decreased the potential fibrinolytic activity of ECs. The 6 hours conditioned medium obtained from the coculture system between monocytes and either ECs or paraformaldehyde-fixed ECs had almost the same effect on the other ECs to produce PAI-1 and t-PA as monocytes that were direct contact with ECs. In addition, this effect was specifically inhibited by using two antibodies against interleukin-1 beta and tumor necrosis factor-alpha. These results indicate that interleukin-1 beta and tumor necrosis factor-alpha induced by the coculture are mostly responsible for decreasing the fibrinolytic activity of ECs.

Cells, Cultured↗
PubMed1997

Activation of human monocytes for enhanced production of interleukin 8 during transendothelial migration in vitro.

Interleukin-8 (IL-8) is a chemokine for polymorphonuclear leukocytes (PMNs) and lymphocytes, which promotes the extravasation of these inflammatory cells. In this study, we investigated IL-8 synthesis induced by the adhesive interaction between monocytes and endothelial cells during transmigration and the capacity of transmigrated monocytes to produce IL-8. Cocultured human monocytes and human umbilical vein endothelial cell (HUVEC) monolayers induced the synergistic production of IL-8, compared with cultures of either monocytes or HUVEC monolayers alone. Coculture-induced IL-8 production almost doubled after HUVECs were stimulated with IL-1 beta. The induced IL-8 mRNA expression was consistent with the protein data, indicating the de novo synthesis of IL-8 by the coculture. Monoclonal antibodies (mAbs) against IL-8 inhibited the transendothelial chemotactic activity of the supernatants for PMNs by 55%. Immunohistochemistry revealed that both adherent and transmigrated monocytes and unstimulated HUVECs expressed IL-8 protein, whereas nonadherent monocytes did little. Transmigrated monocytes spontaneously secreted a 3.8-fold greater amount of IL-8 than the initial monocytes. Coculture-induced IL-8 production was inhibited about 30% by polyclonal Abs against IL-alpha, IL-1 beta, or tumor necrosis factor alpha, while it was not affected by mAbs against intercellular adhesion molecule 1 or vascular cell adhesion molecule 1. The results suggested that adhesive interaction during the transmigration of monocytes through HUVEC monolayers activates both cell types to produce IL-8 and that transmigrated monocytes are capable of producing ample IL-8.

Antibodies, Monoclonal↗
PubMed1997

Detection of large macrophage colony forming cells in the peripheral blood of patients with rheumatoid arthritis.

OBJECTIVE: To test for the presence of colony forming cells, that form large macrophage colonies (> 2.5 mm in diameter, > 10,000 cells), in the peripheral blood of patients with rheumatoid arthritis (RA) and to determine its association with the clinical and laboratory features of RA. METHODS: Peripheral blood mononuclear cells (PBMC) from 96 patients with RA and 20 healthy controls were assayed for in vitro colony formation. In addition, PBMC from 38 patients with other rheumatic diseases including systemic lupus erythematosus (SLE), progressive systemic sclerosis (SSc), and polymyositis/dermatomyositis (PM/DM); 23 patients with infectious inflammatory diseases were also assayed. RESULTS: Large macrophage colony forming cells were detected in the peripheral blood of 19% of patients with RA (18/96), but not in that of healthy controls. In addition, these cells were detected in the peripheral blood of 11 of the 38 patients with other rheumatic disease (7/13 SSc and 4/11 PM/DM), but not in the 23 patients with infectious diseases. In the patients with RA, interstitial lung disease was significantly more frequently observed among patients in whom colony forming cells were found than among those in whom they were not found (p < 0.001). CONCLUSION: Based on the size of the colonies they formed, the macrophage colony forming cells detected in patients with RA probably corresponded to primitive hematopoietic progenitor cells, defined as high proliferative potential colony forming cells (HPP-CFC). Our observations provide preliminary evidence of the appearance of HPP-CFC in the circulation during inflammation of RA, and during that in other rheumatic diseases such as SSc and PM/DM, and of the association of HPP-CFC with interstitial lung disease in patients with RA.

Adult↗
PubMed1996

Selective accumulation of anti-histone antibodies in glomeruli of lupus-prone lpr mice.

Immunoglobulins were eluted from glomeruli of 50 lupus-prone, lpr mice and their physicochemical properties and specificity were compared with those in sera pooled from the same mice. Although immunoglobulins in glomeruli had higher isoelectric points than those in sera, there were no appreciable differences in the relative contents of neutral and acidic immunoglobulins between them. The proportion of IgG3 subclass was slightly higher in glomerular than serum immunoglobulins. Both anti-single-stranded and anti double-stranded DNA antibodies were twofold higher in glomerular than serum immunoglobulins, while anti-Sm antibodies were not recovered in glomerular eluate despite their high activity in serum. Antibodies in glomerular eluate reacted most strongly with histones, especially with core histones, while those in sera bound preferentially with histone H1, Sm-B, -B', and -D antigens. Since histones are very basic, they would have a higher affinity for negatively charged glomerular constituents, leading to an in situ formation of immune complexes involving fixed histones and their binding with antibodies for the induction of nephritides. Otherwise, such immune complexes themselves might retain positive charges sufficient for an affinity with the glomerular basement membrane. These results indicate that histone-anti-histone antibody system may play a role in the perpetuation of murine lupus nephritis.

Animals↗
PubMed1996

Nitric oxide attenuates adhesion molecule expression in human endothelial cells.

Leukocyte adhesion to vascular endothelium is a crucial step in the early stages of atherosclerosis, which may be mediated by the interaction of adhesion molecules expressed on the surfaces of both cell types. In this study, we investigated the effects of nitric oxide (NO) on the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in human umbilical vein endothelial cells (HUVECs). ICAM-1 and VCAM-1 protein and mRNA expression were determined by cellular ELISA and Northern blot analysis, respectively. Both ICAM-1 and VCAM-1 expression were increased markedly by interleukin-1 beta (IL-1 beta). This IL-1 beta-mediated induction of ICAM-1 and VCAM-1 expression was significantly inhibited in the presence of a NO donor 3-morpholino-sydnonimine (SIN-1) in a dose-dependent manner. The inhibitory effect of SIN-1 was abolished in the presence of a NO scavenger haemoglobin, while addition of 8-bromo-cGMP showed no significant effect on IL-1 beta-induced ICAM-1 or VCAM-1 expression. Northern blot analysis showed that IL-1 beta markedly increased ICAM-1 and VCAM-1 mRNA expression, while SIN-1 decreased the accumulation of these transcripts induced by IL-1 beta. These results suggest that NO could prevent the focal adhesion and accumulation of leukocytes through the inhibition of ICAM-1 and VCAM-1 expression in endothelial cells.

Cell Adhesion↗
PubMed1996

Monocyte-endothelial cell interaction induces expression of adhesion molecules on human umbilical cord endothelial cells.

OBJECTIVE: The adhesive interaction of monocytes and endothelial cells has been implicated as a regulatory signal in the cell activation that is involved in the pathogenesis of atherosclerosis. We investigated the effect of monocyte-endothelial cell interaction on the expression of adhesion molecules, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), in human umbilical cord vein endothelial cells (HUVECs). METHODS: ICAM-1 and VCAM-1 protein and mRNA expression were determined by cellular ELISA and Northern blot analysis, respectively. RESULTS: The addition of unstimulated human monocytes, as well as interleukin-1 beta (IL-1 beta: 25 U/ml) and tumor necrosis factor-alpha (TNF: 100 U/ml), to HUVECs rapidly induced the expression of ICAM-1 and VCAM-1 protein and mRNA in HUVECs, whereas the addition of polymorphonuclear leukocytes (PMNs) had no significant effect on their expression. The induction of ICAM-1 and VCAM-1 by the co-culture of HUVECs and monocytes was significantly, but partially, inhibited by the combination of anti-IL-1 alpha, anti-IL-1 beta and anti-TNF Abs. Actinomycin D and genistein, but not calphostin C, also significantly inhibited the co-culture-induced adhesion molecule expression. CONCLUSIONS: These results suggest that the monocyte-endothelial cell interaction induces the expression of ICAM-1 and VCAM-1 in endothelial cells partially through the production of IL-1 and TNF. These findings also suggest that the monocyte-endothelial interaction further augments their interaction through the up-regulation of endothelial adhesion molecules, as a positive feedback mechanism.

Arteriosclerosis↗
PubMed1996

Early-stage rheumatoid arthritis: diagnostic accuracy of MR imaging.

PURPOSE: To investigate the role of magnetic resonance (MR) imaging in diagnosing early rheumatoid arthritis (RA). MATERIALS AND METHODS: Twenty patients (three men, 17 women; age range, 21-72 years) with clinically and radiologically proved RA underwent evaluation to define an MR imaging criterion for diagnosing synovial inflammation due to RA. Twenty-seven patients (16 with RA, 11 without RA [control patients]; three men, 24 women; age range, 19-75 years) suspected to have early RA but without radiographic abnormalities underwent evaluation to test the accuracy of using the criterion to diagnose RA. In each patient, coronal, fat-suppressed, and gadolinium contrast material-enhanced, T1-weighted images of both hands were obtained. RESULTS: The MR imaging criterion was periarticular contrast material enhancement of the wrists or the metacarpophalangeal and/or proximal interphalangeal joints in both hands. In the diagnosis of early RA, sensitivity and negative predictive value were both 100%, specificity was 73%, and accuracy was 89%. CONCLUSION: MR imaging is extremely useful in diagnosing early RA.

Adult↗