Biomedical subjects

T Matsuguchi

Publications and source records attributed to T Matsuguchi.

At least 37 records · Page 2Linked to original sources

PubMed1999

Prostaglandin E(1) protects against liver injury induced by Escherichia coli infection via a dominant Th2-like response of liver T cells in mice.

Prostaglandin E series (PGEs) are known to protect against lipopolysaccharide (LPS)-induced liver injury by down-regulating the production of inflammatory cytokines. We show here a novel mechanism whereby prostaglandin E(1) protects mice against liver injury after Escherichia coli infection. Prostaglandin E(1) administration suppressed circulating interleukin 12 (IL-12) levels but increased the IL-10 production after E. coli challenge. Furthermore, prostaglandin E(1)-alpha-cyclodextrin (PGE(1)) shifted the Th1/Th2 balance of CD3(intermediate) IL-2Rbeta(+) T cells in the liver to a dominant Th2-like response. Neutralization of endogenous IL-4 by administration of anti-IL-4 monoclonal antibody (mAb) diminished the inhibitory effect of prostaglandin E(1) on liver injury after E. coli challenge. These results suggested that the Th2-like response of liver T cells may be at least partly involved in the mechanism whereby prostaglandin E(1) protects against E. coli-induced liver injury.

Alprostadil↗

PubMed1999

Endogenous IL-15 might be responsible for early protection by natural killer cells against infection with an avirulent strain of Salmonella choleraesuis in mice.

Interleukin (IL)-15 is a novel cytokine with growth factor activity for T cells, B cells, and natural killer cells (NK cells). We investigated the role of IL-15 in the host defense against infection with avirulent Salmonella choleraesuis strain 31N-1 cured of 50-kb virulent plasmid. IL-15 was abundantly expressed at transcription and protein levels in macrophages infected with S. choleraesuis 31N-1. The number of NK cells in the infected sites was increased during the course of infection coincident with IL-15 production. Anti-IL-15 mAb administration inhibited the emergence of NK cells and interferon-gamma (IFN-gamma) production in serum after infection with S. choleraesuis 31N-1 and concurrently impaired the clearance of the bacteria. These results suggested that IL-15 might be responsible for protection against avirulent S. choleraesuis infection at early stage of infection through activation of NK cells in the infected sites.

Animals↗

PubMed1998

Regulation of myeloid cell growth by distinct effectors of Ras.

To examine the biochemical pathways by which activated Ha-Ras(G12V) (Ha-RasV12) induces factor-independent growth of myeloid cells, Ha-Ras effector loop mutations, including Y40C, T35S, and E37G, were analysed in a mouse factor-dependent myeloid cell line, WT19. Expression of a single effector loop mutant, Ha-Ras(G12V, Y40C) (Ha-RasV12C40), inhibited factor-withdrawal apoptosis, suggesting that activation of the phosphatidylinositol 3'-kinase (Pl3K) pathway is essential to prevent cell death. Neither Ha-Ras (G12V, T35S) (Ha-RasV12S35), which activates the Rafl signaling pathway, nor Ha-Ras(G12V, E37G) (Ha-RasV12G37), which stimulates the RalGDS pathway, did not have significant effects on factor-withdrawal apoptosis of myeloid cells. Although Ha-RasV12C40 inhibited apoptosis, it did not stimulate entry into the cell cycle. Cell lines containing the combination of Ha-RasV12G37 and Ha-RasV12C40 were capable of factor-independent cell growth, while expression of the other combinations of the Ha-Ras effector mutants were not. The combined expression of Bcl-2 and Ha-RasV12G37 was not sufficient to stimulate factor independent growth, suggesting that Ha-RasV12C40 activates additional signals, besides blocking apoptosis, which are critical for factor-independent growth of myeloid cells. In factor-starved myeloid cells, inducible expression of Ha-RasV12G37 results in decreased level of p27Kip1 protein, a cyclin-dependent kinase inhibitor (CKI). These data suggest that the factor-independent growth of myeloid cells requires the activation of at least two pathways, one inhibiting factor-withdrawal apoptosis, and another causing cell cycle progression.

Amino Acid Substitution↗

PubMed1998

Cytoplasmic domains of the human granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor beta chain (hbetac) responsible for human GM-CSF-induced myeloid cell differentiation.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) regulates differentiation, survival, and proliferation of myeloid progenitor cells. The biologic actions of GM-CSF are mediated by its binding to the alpha and beta subunits of the GM-CSF receptor (GM-CSFRalpha and betac, respectively). To determine whether identical regions of the betac protein mediate both cell growth and differentiation, we expressed cDNA constructs encoding the human wild-type (897 amino acids) and truncated betac (hbetac) subunits along with the wild-type human GM-CSFRalpha subunit in the murine WT19 cell line, an FDC-P1-derived cell line that differentiates toward the monocytic lineage in response to murine GM-CSF. Whereas the WT19 cell line carrying the C-terminal deleted hbetac subunit of 627 amino acids was still able to grow in human GM-CSF (hGM-CSF), 681 amino acids of the hbetac were necessary for cell differentiation. The addition of hGM-CSF to WT19 cell lines containing the hbetac627 subunit stimulated the phosphorylation of ERK (extracellular signal-regulated kinase) and induced the tyrosine-phosphorylation of SHP-2 and STAT5, suggesting that the activation of these molecules is insufficient to mediate the induction of differentiation. A point mutation of tyrosine 628 to phenylalanine (Y628F) within hbetac681 abolished the ability of hGM-CSF to induce differentiation. Our results indicate that the signals required for hGM-CSF-induced differentiation and cell growth are mediated by different regions of the hbetac subunit.

Animals↗

PubMed1998

Interleukin-15 may be responsible for early activation of intestinal intraepithelial lymphocytes after oral infection with Listeria monocytogenes in rats.

Exogenous interleukin-15 (IL-15) stimulates intestinal intraepithelial lymphocytes (i-IEL) from mice to proliferate and produce gamma interferon (IFN-gamma) in vitro. To determine whether endogenous IL-15 is involved in activation of i-IEL during intestinal infection, we examined IL-15 synthesis by intestinal epithelial cells (i-EC) after infection with Listeria monocytogenes in rats. In in vitro experiments, invasion of L. monocytogenes into IEC-6 cells, a rat small intestine epithelial cell line, evidently induced IL-15 mRNA expression coincident with nuclear factor kappaB (NF-kappaB) activation, which is essential for IL-15 gene expression. IL-15 synthesis was detected in rat i-EC on day 1 after an oral inoculation of L. monocytogenes in vivo. The numbers of T-cell receptor (TCR) gamma delta+ T cells, NKR.P1(+) cells, and CD3(+) CD8(+) alpha alpha cells in i-IEL were significantly increased on day 1 after oral infection. The i-IEL from infected rats produced larger amounts of IFN-gamma upon stimulation with immobilized anti-TCR gamma delta or anti-NKR.P1 monoclonal antibodies. These results suggest that IL-15 produced by i-EC may stimulate significant fractions of i-IEL to produce IFN-gamma at an early phase of oral infection with L. monocytogenes.

Animals↗

PubMed1997

The cytoplasmic domain of granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor alpha subunit is essential for both GM-CSF-mediated growth and differentiation.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) regulates differentiation, survival, and proliferation of colony-forming unit-granulocyte-macrophage progenitor cells. The biologic actions of GM-CSF are mediated by binding to a specific receptor consisting of two chains designated as alpha and beta subunits. We have demonstrated that the murine FDC-P1-derived cell line WT-19 transfected with the human GM-CSF receptor alpha and beta subunits (GM-CSFRalpha and beta) can be induced to differentiate by the addition of human GM-CSF (hGM-CSF). By expressing a series of GM-CSFRalpha mutants in WT19 cells, we have determined the amino acid domains of the GM-CSFRalpha cytoplasmic domain that regulate cell differentiation, proliferation, and survival. We found that the membrane proximal proline-rich domain and adjacent 16 residues are essential for both hGM-CSF-dependent cell proliferation and differentiation. In contrast, the C-terminal region of the GM-CSFRalpha cytoplasmic domain was not necessary for cell differentiation mediated by hGM-CSF, but the removal of this region severely impaired the ability of hGM-CSF to support cell survival. While the activation of JAK2, Shc, Erk, and STAT5 proteins correlated with hGM-CSF-mediated cell growth, cellular differentiation occurred in the absence of activation of these signal transduction pathways.

Adaptor Proteins, Signal Transducing↗

PubMed1996

Effect of cilostazol, a novel anti-platelet drug, on restenosis after percutaneous transluminal coronary angioplasty.

The possible preventive effect of cilostazol, a novel anti-platelet drug, on restenosis after successful percutaneous transluminal coronary angioplasty (PTCA) was examined. One hundred and two consecutive patients, who underwent successful PTCA, were followed for 3 to 6 months. To prevent restenosis, 46 patients (60 PTCA sites) were treated with cilostazol alone (200 mg/day) (cilostazol group) and the remaining 56 (61 PTCA sites) were treated with other anti-platelet drugs and/or warfarin potassium (control group). Restenosis was defined as a more than 50% loss of the initial gain of the coronary diameter achieved by PTCA. Cilostazol did not significantly reduce the patient or lesion restenosis rate; the patient restenosis rate was 32% in the control group and 22% in the cilostazol group (P = 0.24), and the lesion restenosis rate was 30% in the control group and 23% in the cilostazol group (P = 0.44). However, the lesion non-progression rate, which was defined as the incidence of lesions with either no change or regression of coronary stenosis at the PTCA site, was significantly greater with cilostazol (37%) than in the control group (16%) (p < 0.05). Although cilostazol failed to show a significant reduction in restenosis after PTCA, the present results suggest that a further trial with a larger number of patients is needed to confirm its usefulness.

Aged↗

PubMed1996

Granulocyte activation in restenosis after percutaneous transluminal coronary angioplasty.

To examine whether or not granulocyte activation is involved in restenosis after percutaneous transluminal coronary angioplasty (PTCA), we prospectively followed the time course of the plasma level of granulocyte elastase, which is an index of granulocyte activation, before and after successful angioplasty in 43 consecutive patients. Restenosis was defined as a more than 50% loss of the initial gain in the coronary diameter achieved by PTCA with more than a 50% resultant stenosis in the follow-up coronary arteriography performed 3 months after PTCA. There was no difference in the level of granulocyte elastase between the 2 groups with (n = 15) and without (n = 28) restenosis before, the day after and 1 month after PTCA. However, 3 months after PTCA, the level of granulocyte elastase was significantly higher in the group with restenosis than in that without restenosis (171 +/- 13 vs 147 +/- 6 mg/l, P < 0.05). The level of granulocyte elastase at 3 months after PTCA also correlated significantly with the percent luminal stenosis at the angioplasty site (P < 0.05). These results suggest that granulocyte activation may be involved in restenosis after PTCA.

Adult↗

PubMed1996

[Rapidly progressive T-cell angiocentric lymphoma with CD56+ phenotype involving bilateral orbits and skin in a patient with anti-HTLV-I antibody].

A 57-year-old woman was admitted to our hospital complaining of left exophthalmos in July, 1991. Biopsy specimen of a tumor in the left orbit suggested an inflammatory pseudotumor. The orbit was irradiated and the exophthalmos disappeared. During admission, an erythema was noted on her anterior chest wall. After discharge, right exophthalmos and generalized skin eruptions developed. The skin eruption on her anterior chest wall was histopathologically diagnosed as angiocentric lymphoma and she was readmitted. Since her serum was positive for anti-HTLV-I antibody, adult T-cell leukemia/lymphoma was suspected. Chemotherapy yielded limited relief of the right exophthalmos and transient fading of the skin eruptions. She died due to progression of the disease. Close examination of the skin eruption on the calf revealed that the lymphoma cells were CD56-positive immunohistochemically and electron microscopy revealed that they had large membrane-bound granules. Rearrangement of the T-cell receptor beta chain gene was observed. Incorporation of HTLV-I proviral DNA was not observed. Re-examination of the left orbital tumor confirmed the infiltration of these lymphoma cells. This is a rare case of T-cell lymphoma with NK cell phenotype involving orbits and skin, and showing a rapid clinical course.

CD56 Antigen↗

PubMed1995

Tyrosine phosphorylation of p95Vav in myeloid cells is regulated by GM-CSF, IL-3 and steel factor and is constitutively increased by p210BCR/ABL.

Vav is a recently described proto-oncogene expressed only in hematopoietic cells which contains an SH2 and two SH3 domains and shares homology with the Dbl GDP-GTP exchange factor and BCR. p95Vav is phosphorylated on tyrosine residues in response to stimulation of the T cell antigen receptor, cross-linking of IgE or IgM receptors and stimulation of immature hematopoietic cells by Steel factor. Monoclonal antibodies to human Vav were generated and used to examine the events which regulate tyrosine phosphorylation of p95Vav in myeloid cells. In the factor-dependent MO7e cell line, p95Vav was rapidly phosphorylated on tyrosine residues in a dose- and time-dependent manner by GM-CSF, IL-3 and Steel factor. Introduction of the BCR/ABL oncogene into this cell line resulted in factor-independent proliferation and constitutive phosphorylation of p95Vav. Tyrosine phosphorylation of p95Vav was also substantially increased by treatment of cytokine-deprived cells with the tyrosine phosphatase inhibitor sodium vanadate. Since many of the cytokines known to induce tyrosine phosphorylation of p95Vav are also known to activate JAK family tyrosine kinases, we looked for an interaction of p95Vav with JAK kinases. p95Vav co-precipitated with JAK2 in MO7e cells stimulated with GM-CSF, but not in unstimulated cells. Also, JAK2 was found to be constitutively associated with p95Vav in vivo when expressed at high levels in insect cells using baculovirus vectors. A fusion protein consisting of glutathione-S-transferase and the SH2 domain of p95Vav (GST-Vav-SH2) precipitated JAK2, suggesting that this interaction is mediated by the SH2 domain of p95Vav.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Phylogeny of Sym plasmids of rhizobia by PCR-based sequencing of a nodC segment.

To understand the host specificity of rhizobia and the relationship between the evolution of Sym plasmids and that of host plants, we determined partial nodC sequences of 10 representative rhizobium strains and then constructed an evolutionary tree for the deduced amino acid sequences with four published sequences. These coding sequences yield a phylogenetic tree similar to that for leghemoglobin of host plants, suggesting that the evolution of common nodulation genes may be linked to host legume evolution and speciation.

Amino Acid Sequence↗

PubMed1995

Remarkable N2-fixing bacterial diversity detected in rice roots by molecular evolutionary analysis of nifH gene sequences.

To demonstrate the extent of phylogenetic diversity of diazotrophic bacteria associated with rice roots, we characterized phylogenetically 23 nifH gene sequences obtained by PCR amplification of mixed organism DNA extracted directly from rice roots without culturing the organisms. The analyses document the presence of eight novel NifH types, which appear to be a variety of significant components of the diazotrophic community, dominated mainly by proteobacteria.

Amino Acid Sequence↗

PubMed1995

Genetic diversity of N2-fixing bacteria associated with rice roots by molecular evolutionary analysis of a nifD library.

The rhizosphere of wetland rice has significant N2-fixing activity. It has been suggested that N2 fixation in the rice root zone is associated with the activity of various N2-fixing heterotrophic bacteria that inhabit the rice rhizosphere. Because of the generic diversity, many different isolation media and conditions are required to count and isolate these bacteria. In an attempt to overcome any bias from culture-dependent methods we amplified nifD segments from crude rice root DNA by the polymerase chain reaction. The nifD fragments were then cloned into a pT7 Blue T-vector to construct a nifD library. Sixteen cloned nifD genes chosen at random from the library were sequenced. A comparison with published sequences indicated the presence of seven novel groups of NifD proteins, which implies the existence of at least seven components in the diazotrophic community of rice roots, dominated mainly by proteobacteria. We also observed genetic variability within the clusters, which suggests the coexistence of many closely related bacterial lineages. However, we did not find Azospirillum-like nifD clones, although many reports indicated the widespread presence of Azospirillum spp. Therefore, it remains to be clarified whether Azospirillum species are the widespread N2-fixing bacteria in rice roots.

Amino Acid Sequence↗

PubMed1995

The SH2 domain of ABL is not required for factor-independent growth induced by BCR-ABL in a murine myeloid cell line.

Chronic myelogenous leukemia (CML) is characterized by the presence of a specific chromosomal translocation between the long arms of chromosomes 9 and 22 that results in the fusion of BCR encoded sequences upstream of exon 2 of c-ABL. This fusion gene produces a 210-kDa chimeric BCR-ABL protein that has elevated tyrosine kinase activity. Several substrates of this activated tyrosine kinase have been reported. However, their necessity for the transforming functions of BCR-ABL has not been determined. A specific deletion of the SH2 domain of ABL was created to determine whether this mutation would alter the ability of BCR-ABL to induce factor-independent growth of a murine myeloid cell line and to determine whether the SH2 domain mediates the interaction of BCR-ABL with any of its substates. Our results indicate that the SH2 domain of BCR-ABL is not required for the induction of growth factor independence and is not required for the association of BCR-ABL with rasGAP or SHC. However, myeloid cells expressing this mutant lack the tyrosine phosphorylation of a 62-kDa rasGAP associated protein.

Animals↗

PubMed1994

Shc phosphorylation in myeloid cells is regulated by granulocyte macrophage colony-stimulating factor, interleukin-3, and steel factor and is constitutively increased by p210BCR/ABL.

Granulocyte macrophage colony-stimulating factor, interleukin-3, and steel factor induce proliferation of hematopoietic cells through binding to specific, high affinity, cell surface receptors. However, little is known about post-receptor signal transduction pathways. Here we report that an SH2 domain containing protein previously implicated in the activation of p21ras, Shc, is transiently tyrosine phosphorylated in myeloid cells after stimulation with granulocyte macrophage colony-stimulating factor, interleukin-3, or steel factor. Also, Shc was found to be constitutively tyrosine phosphorylated in myeloid cell lines made factor independent by expression of p210BCR/ABL. A Shc-associated 140-kDa protein was identified, which was phosphorylated on tyrosine residues transiently after cytokine stimulation and constitutively after expression of p210BCR/ABL. These findings suggest that Shc could play an important role in a signal transduction pathway, which leads to the proliferation of myeloid cells.

Adaptor Proteins, Signal Transducing↗

PubMed1993

Accuracy of electronic digital calipers compared with quantitative angiography in measuring coronary arterial diameter.

BACKGROUND: Quantitative angiography is the accepted method for measuring coronary luminal diameter. Electronic digital calipers have been used to assess arterial diameters in vasomotor function studies and after interventional procedures. However, careful validation of calipers against quantitative angiography has not been described. METHODS AND RESULTS: We used digital calipers and quantitative angiography to measure 517 arterial diameters (88 nonstenotic segments) in 24 transplant patients undergoing vasomotor function studies with acetylcholine and nitroglycerin, 20 stenoses in 14 patients with coronary artery disease, and 15 stenoses in 15 patients before and after excimer laser-facilitated coronary angioplasty and at 6 months' follow-up. In nonstenotic arterial segments ranging in size from 0.6 to 3.5 mm, calipers overestimated diameters measured by quantitative angiography by 0.29 +/- 0.21 mm (mean +/- SD) (limits of agreement, -0.13 to 0.71 mm). However, when the vasomotor responses were expressed as percent diameter change, the two methods did not differ significantly (-1 +/- 10%; limits of agreement, -21% to 19%). In the 35 stenoses measured before intervention and 30 stenoses measured after intervention, calipers and quantitative angiography differed by 3 +/- 9% (limits of agreement, -15% to 21%) across a range of stenosis severity (11% to 80%). Repeat caliper measurements by the same observer of the percent diameter change in the transplant patients and the percent stenosis in the coronary artery disease patients led to standard deviations of the differences of 9.3% and 7.6%, respectively. Two different observers recorded percent diameter change and percent stenosis that differed with standard deviations of 9.6% and 7.8%, respectively. CONCLUSIONS: Quantitative angiography and electronic digital calipers produce similar relative changes in arterial diameters and percent stenosis in a broad range of severities. Digital calipers thus are a rapid and convenient alternative to computerized quantitative angiography in certain research studies and clinical practice of assessing stenosis severity.

Coronary Angiography↗

PubMed1993

Intracellular magnesium deficiency in acute myocardial infarction.

It has been hypothesized that intracellular magnesium deficiency is a pathogenetic factor in acute myocardial infarction. This study examined the time course of changes in the erythrocyte magnesium concentration and the correlation between the erythrocyte magnesium concentration and the severity of acute myocardial infarction in 49 consecutive patients with transmural acute myocardial infarction. The data were compared with results from 20 control patients without ischemic heart disease. The erythrocyte magnesium concentration (mg/dl) decreased significantly during the acute phase of the infarction (4.86 +/- 0.09 on day 1, 4.89 +/- 0.10 on day 2 and 4.86 +/- 0.10 on day 3 versus 5.26 +/- 0.19 for controls, all P < 0.05) and then normalized gradually to 5.25 +/- 0.10 on day 28. The serum magnesium concentration (mg/dl) also decreased significantly during the acute phase of the infarction (1.93 +/- 0.04 on day 1 and 2.11 +/- 0.03 on day 2 versus 2.26 +/- 0.08 for controls, all P < 0.05), before recovering to 2.28 +/- 0.06 on day 28. There were significant correlations between the erythrocyte magnesium concentration on day 1 and maximal values of serum cardiac enzymes (r = -0.30 for creatine kinase, r = -0.34 for glutamic oxaloacetic transaminase and r = -0.57 for lactate dehydrogenase, all P < 0.05). Moreover, the erythrocyte magnesium concentration was significantly lower in patients with (4.32 +/- 0.08 mg/dl, n = 13) than in those without (5.06 +/- 0.09 mg/dl, n = 36, P < 0.0001) serious arrhythmias. These data indicate that intracellular magnesium deficiency is involved in the acute phase of myocardial infarction.

Adult↗

PubMed1992

Alcohol-induced sinus bradycardia and hypotension in patients with syncope.

We observed 2 cases of repeated episodes of syncope after alcohol ingestion. Both patients were light drinkers and had carotid sinus hypersensitivity. In both cases, alcohol loading tests repeatedly induced sinus bradycardia and hypotension 1.0-1.5 hours after drinking alcohol. Atropine was effective in improving symptoms. A loading test using a glucose solution of equivalent osmolarity and volume was negative. Acute alcohol ingestion usually increases heart rate with variable effects on blood pressure. However, our 2 cases exhibited unusual alcohol-induced sinus bradycardia and hypotension, suggesting a paradoxical increase in parasympathetic activity and/or decrease in sympathetic activity.

Aged↗