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K Matsuno

Publications and source records attributed to K Matsuno.

At least 19 recordsLinked to original sources
PubMed2003

Charge ordering and spin frustration in AlV2-x CrxO4.

The relationship between charge and spin degrees of freedom in a geometrically frustrated system, AlV2-xCrxO4 spinel, is investigated. Upon Cr doping, the charge-ordered phase of AlV2O4 is rapidly suppressed and a charge-disordered phase grows up instead. It is found that the magnetic ground state is a spin-glass state dominated by geometrical frustration for both phases, but larger spin entropy remains down to low temperatures in the charge-ordered phase, possibly owing to its two-dimensional character.

Journal Article↗
PubMed2003

Ectopic synaptogenesis during retinal degeneration in the royal college of surgeons rat.

Rod photoreceptor-specific mutations cause ectopic synapses to form between cone photoreceptor terminals and rod bipolar cell dendrites in degenerating retinas of rhodopsin transgenic (P347L) pigs and retinal degeneration mice. Since the mutations occur in rod photoreceptor-specific genes in these two models, it is not known if ectopic synaptogenesis occurs specifically due to some rod photoreceptor cell-autonomous properties of a mutation or as a general consequence of photoreceptor degeneration. In the Royal College of Surgeons (RCS) rat, a mutation in the receptor tyrosine kinase gene, Mertk, causes failure of the retinal pigment epithelial (RPE) cells to phagocytose shed photoreceptor outer segments; subsequently, both rod and cone photoreceptors die. The non-phagocytic phenotype of the RCS rat is RPE cell-autonomous and the photoreceptors degenerate secondarily. Here we show that in 35-day-old RCS rats, where a majority of rod and cone photoreceptors remained, rod bipolar cell dendrites had abnormal (flat-contact type) synaptic contacts with rod and cone terminals. Demonstration of ectopic synapses in the RCS rat suggested that ectopic synaptogenesis could occur as a result of photoreceptor degeneration, even when the rods and cones were developmentally normal. This further supported the hypothesis that ectopic synaptogenesis may be a common step in the disease progression of different forms of retinal degeneration that include photoreceptor death as a feature, such as retinitis pigmentosa.

Animals↗
PubMed2002

Wine stimulates gastric acid secretion in isolated rabbit gastric glands via two different pathways.

BACKGROUND & AIMS: Alcoholic beverages such as beer and wine are well known to potently stimulate gastric acid secretion, most probably through an increase in circulating gastrin level. The present study examined whether or not wine stimulates gastric acid secretion by a direct effect on parietal cells, enterochromaffin-like (ECL) cells or both. METHODS: Gastric mucosa was isolated from female Japanese white rabbits and gland specimens were prepared by the collagenase digestion method. Acid secretion was assessed by gland accumulation of [14C] aminopyrine. The effects of red wine, ethanol, non-alcoholic wine and drugs were determined by incubating gastric glands with aminopyrine. Radioactivity in solubilized glands was determined by a liquid scintillation counting. RESULTS: Neither wine nor ethanol (diluted 1 : 10(2) to 1 : 10(4)) had any effect on gastric acid secretion, whereas non-alcoholic wine stimulated acid secretion in a dose-dependent manner. All substances, however, significantly stimulated gastric acid secretion in IBMX (phosphodiesterase inhibitor)-pretreated glands. S-0509 (a CCK-2 receptor antagonist) and atropine had no effect on acid secretion stimulated by wine, ethanol or non-alcoholic wine in IBMX-pretreated glands. Famotidine and omeprazole significantly inhibited the acid secretion resulting from all of the above stimulants. BAPTA (an intracellular Ca2+ chelator) inhibited acid secretion stimulated with wine or ethanol in a dose-dependent manner, but did not inhibit secretion stimulated by non-alcoholic wine. CONCLUSIONS: Wine was found to stimulate gastric acid secretion in gastric glands via two pathways, by an ethanol-induced increase in the concentration of intracellular Ca2+ in parietal cells, and by histamine release from ECL cells potentially induced by constituents present in wine.

Animals↗
PubMed2001

Role of Deltex-1 as a transcriptional regulator downstream of the Notch receptor.

Intercellular signaling through the cell-surface receptor Notch plays important roles in a variety of developmental processes as well as in pathogenesis of some human cancers and genetic disorders. However, the mechanisms by which Notch signals are transduced into cells still remain elusive. Here we investigated the signaling mechanisms for Notch in the cell fate control of neural progenitor cells. We show that Deltex-1 (DTX1), a mammalian homolog of Drosophila Deltex, mediates a Notch signal to block differentiation of neural progenitor cells. We found that a significant fraction of DTX1 proteins were localized in the nucleus and physically interacted with the transcriptional coactivator p300. Through its binding to p300, DTX1 inhibited transcriptional activation by the neural-specific helix-loop-helix-type transcription factor MASH1, and this mechanism is likely responsible for the differentiation inhibition of neural progenitor cells. Our results further suggest that DTX1 regulates transcription independently of the previously characterized Notch signaling pathway involving RBP-J and HES1/HES5. Thus, DTX1 serves as an important signaling component downstream of Notch that regulates transcription in the nucleus.

Animals↗
PubMed2001

Trafficking of host- and donor-derived dendritic cells in rat cardiac transplantation: allosensitization in the spleen and hepatic nodes.

BACKGROUND: Kinetics and role of host and donor dendritic cells (DCs) in transplantation immunity are still ill-defined. Using a rat cardiac transplantation model, we studied DC trafficking and sites for allosensitization. METHODS: Host and donor DCs were defined as host- or donor-type class II major histocompatibility complex antigen single-positive cells by double-immunostaining. Proliferative response of both donor and host cells were also analyzed. RESULTS: Host DCs were recruited to the graft soon after transplantation. These cells represented definitive precursors because of high labeling index by a continuous bromodeoxyuridine infusion, their small round shape, and their putative bone marrow origin. Donor interstitial DCs showed a significant self-replicating capability. Both recruited host DCs in a regraft experiment and donor DCs preferentially performed blood-borne migration to the T-cell area of host spleen. Furthermore, they also migrated to the T-cell area of hepatic lymph nodes after executing the sinusoids-lymph translocation as a novel pathway for these DCs. Selectively at their migration sites, a strong T-cell proliferative response occurred, which preceded that in the graft tissues. Removal of spleen and hepatic lymph nodes significantly prolonged the mean graft survival time. CONCLUSION: We conclude that allogeneic heart transplantation induces the recruitment of host DC precursors to the graft tissues and the blood-borne migration of both recruited host and donor DCs to the host spleen and hepatic nodes where effector cells are predominantly sensitized.

Animals↗
PubMed2001

Crystal structure of Bacillus subtilis isocitrate dehydrogenase at 1.55 A. Insights into the nature of substrate specificity exhibited by Escherichia coli isocitrate dehydrogenase kinase/phosphatase.

Isocitrate dehydrogenase from Bacillus subtilis (BsIDH) is a member of a family of metal-dependent decarboxylating dehydrogenases. Its crystal structure was solved to 1.55 A and detailed comparisons with the homologue from Escherichia coli (EcIDH), the founding member of this family, were made. Although the two IDHs are structurally similar, there are three notable differences between them. First, a mostly nonpolar beta-strand and two connecting loops in the small domain of EcIDH are replaced by two polar alpha-helices in BsIDH. Because of a 13-residue insert in this region of BsIDH, these helices protrude over the active site cleft of the opposing monomer. Second, a coil leading into this cleft, the so-called "phosphorylation" loop, is bent inward in the B. subtilis enzyme, narrowing the entrance to the active site from about 12 to 4 A. Third, although BsIDH is a homodimer, the two unique crystallographic subunits of BsIDH are not structurally identical. The two monomers appear to differ by a domain shift of the large domain relative to the small domain/clasp region, reminiscent of what has been observed in the open/closed conformations of EcIDH. In Escherichia coli, IDH is regulated by reversible phosphorylation by the bifunctional enzyme IDH kinase/phosphatase (IDH-K/P). The site of phosphorylation is Ser(113), which lies deep within the active site crevice. Structural differences between EcIDH and BsIDH may explain disparities in their abilities to act as substrates for IDH-K/P.

Amino Acid Sequence↗
PubMed2001

Regulation by chemokines of circulating dendritic cell precursors, and the formation of portal tract-associated lymphoid tissue, in a granulomatous liver disease.

We have studied the recruitment and roles of distinct dendritic cell (DC) precursors from the circulation into Propionibacterium acnes-induced granulomas in mouse liver. During infection, F4/80(-)B220(-)CD11c(+) DC precursors appeared in the circulation, migrated into the perisinusoidal space, and matured within newly formed granulomas. Recruited DCs later migrated to the portal area to interact with T cells in what we term "portal tract-associated lymphoid tissue" (PALT). Macrophage inflammatory protein 1alpha attracted blood DC precursors to the sinusoidal granuloma, whereas secondary lymphoid organ chemokine (SLC) attracted mature DCs to the newly identified PALT. Anti-SLC antibody diminished PALT expansion while exacerbating granuloma formation. Therefore, circulating DC precursors can migrate into a solid organ like liver, and participate in the granulomatous reaction in response to specific chemokines.

Animals↗
PubMed2001

Evaluation of the retinal nerve fiber layer thickness in eyes with idiopathic macular holes.

PURPOSE: To compare the retinal nerve fiber layer thickness in eyes with idiopathic macular holes and age-matched normal controls using scanning laser polarimeter. METHODS: The retinal nerve fiber layer thickness was measured in 40 eyes of 40 consecutive patients with idiopathic macular hole (stage 1, 10 eyes; stage 2, eight eyes; stage 3, 15 eyes; stage 4, seven eyes) and 40 eyes of 40 age-matched normal controls with a scanning laser polarimeter. The retinal nerve fiber layer thickness within a 10-pixel-wide ellipse located concentrically with the disk and located 1.5-disk diameters from the center of the disk was measured. The mean overall retinal nerve fiber layer thickness of the peripapillary retina, four 90-degree quadrants, and 16 equal sectors of every 22.5 degrees was calculated for both groups. The retinal nerve fiber layer thickness in the two groups was statistically compared. RESULTS: The mean retinal nerve fiber layer thickness measurement for the overall peripapillary retina and for three of the four 90-degree quadrants was not significantly different between the two groups. However, the temporal 90-degree quadrant was significantly thinner in the macular hole group (47.2 versus 54.6 microm, P =.026). For the 16 sectors of 22.5 degrees, the lower three sectors of the four sectors in the temporal quadrant were thinner in the macular hole group (P <.05). CONCLUSIONS: The retinal nerve fiber layer thickness of the papillomacular area is thinner in eyes with idiopathic macular hole than that in normal eyes. The progressive thinning of the retinal nerve fiber layer thickness as the stage of the macular hole advances may suggest that surgery should be done at the earliest stage.

Aged↗
PubMed2001

Neurosteroids stimulate G protein-coupled sigma receptors in mouse brain synaptic membrane.

Dehydroepiandrosterone, its sulfate (DHEAS) and pregnenolone sulfate, representative neurosteroids as well as (+)-pentazocine concentration-dependently stimulated the [35S]GTPgammaS binding in synaptic membranes of mouse prefrontal cortex. These stimulations were blocked by NE-100, a sigma-receptor antagonist, and by progesterone, another type of neurosteroid. The DHEAS-induced stimulation was blocked by the pertussis toxin (PTX)-treatment, and completely recovered by reconstitution of PTX-treated membranes with recombinant G(i1), but not with G(oA). DHEAS also stimulated the [35S]GTPgammaS binding in the coronal sections of mouse brain in NE-100- or progesterone-reversible manner. These findings suggest that some neurosteroids may act on metabotropic sigma receptors, and this study may be the first to show the coupling of neurosteroid binding site and G(i).

Analgesics, Opioid↗
PubMed2001

Murine homologs of deltex define a novel gene family involved in vertebrate Notch signaling and neurogenesis.

Notch signaling plays an important role in cell-fate specification in multicellular organisms by regulating cell-cell communication. The Drosophila deltex gene encodes a modulator of the Notch pathway that has been shown to interact physically with the Ankyrin repeats of Notch. We isolated four distinct cDNAs corresponding to mouse homologs of deltex - mouse Deltex1 (MDTX1), mouse Deltex2 (MDTX2), mouse Deltex2DeltaE (MDTX2DeltaE), and mouse Deltex3 (MDTX3). Deduced amino acid sequences of these four cDNAs showed a high degree of similarity to Drosophila Deltex and its human homolog, DTX1 throughout their lengths, even though they possess distinct structural features. MDTX proteins formed homotypic and heterotypic multimers. We found that these genes were expressed in the central, peripheral nervous system and in the thymus, overlapping with those of mouse Notch1. In mammalian tissue culture cells, overexpression of any of the four mouse deltex homologs suppressed the transcriptional activity of E47, a basic helix-loop-helix (bHLH) protein, in a manner similar to suppression by an activated form of human Notch1 or human DTX1. In addition, overexpression of MDTX2 and MDTX2DeltaE in C2C12 cells under differentiation-inducing conditions suppressed the expression of myogenin, one of the myogenic transcriptional factors; this was also similar to a previously reported activity of constitutively activated Notch. Furthermore, misexpression of any of the MDTX genes in Xenopus embryos resulted in an expansion of the region expressing the neural cell adhesion molecule (N-CAM) gene, a marker for the neuroepithelium. Collectively, our results suggest that these mouse deltex homologs are involved in vertebrate Notch signaling and regulation of neurogenesis.

Amino Acid Sequence↗
PubMed2001

[11C]Raclopride binding was reduced in vivo by sigma(1) receptor ligand SA4503 in the mouse brain, while [11C]SA4503 binding was not by raclopride.

[11C]Raclopride is widely used as a representative dopamine D(2)-like receptor ligand in positron emission tomography (PET) studies, and [11C]1-(3,4-dimethoxyphenethyl)-4-(3-phenylpropyl)piperazine dihydrochloride ([11C]SA4503) is a recently developed selective ligand for mapping sigma(1) receptors in the brain. The striatal uptake of [11C]raclopride in mice was reduced by co-injection of an excess amount of SA4503, in spite of the fact that raclopride had no effect on the brain uptake of [11C]SA4503 as shown in a previous study. The blocking effect of SA4503 on the striatal uptake of [11C]raclopride was dose-dependent, but disappeared by 1 h or 6 h after intraperitoneal injection of SA4503. The brain uptake of [11C]SA4503 was not affected by a dopamine transporter inhibitor GBR 12909, nor was [11C]beta-CIT-FP inhibited by SA4503. The IC(50) values of raclopride for sigma(1) and sigma(2) receptor subtypes measured in vitro were 11800 nM and 4950 nM, respectively, suggesting that the affinity was too low for [11C]raclopride to bind in vivo to sigma receptors. On the other hand, the IC(50) value of SA4503 for dopamine D(2) receptors was 470 nM, that is approximate 1/25 of the affinity of raclopride for the dopamine D(2) receptors. Therefore, possible explanations for the partial blocking effects of SA4503 on the striatal uptake of [11C]raclopride are: (1) an excess amount of SA4503 may reduce the [11C]raclopride uptake due to its low affinity for dopamine D(2) receptors, or (2) SA4503 may enhance endogenous dopamine release, which results in the competitive inhibition of the [11C]raclopride uptake. These findings support that both [11C]raclopride and [11C]SA4503 are selective in vivo ligands for dopamine D(2)-like receptors and sigma(1) receptors, respectively, in spite of the partial blocking effect of SA4503 on the striatal uptake of [11C]raclopride.

Animals↗
PubMed2001

Kupffer cell-mediated recruitment of rat dendritic cells to the liver: roles of N-acetylgalactosamine-specific sugar receptors.

BACKGROUND & AIMS: Tissue recruitment of dendritic cells (DCs) is essential for antigen presentation. This study aimed to examine cellular and molecular mechanisms for DC recruitment to the liver. METHODS: Purified rat DCs were injected into circulation and their traffics were analyzed in normal and Kupffer cell-depleted rats by intravital confocal microscopy and immunohistology. Affinities of DCs to sinusoidal cells were examined by a cell-binding assay. DC precursor recruitment was induced by particulate injection. RESULTS: Both DC precursors and DCs at the antigen-transporting stage could be recruited to the liver, and their majority initially showed a selective binding to Kupffer cells. In the Kupffer cell-depleted rats, DCs could neither be recruited to the liver nor adhere to sinusoidal walls. Pretreatment with varied monosaccharides showed that sugar residues consisting of N-acetylgalactosamine were necessary for this binding. The binding was calcium-dependent, implying the C-type lectin involvement. Furthermore, DCs could endocytose N-acetylgalactosamine polymers in a receptor-specific manner. CONCLUSIONS: The DC-Kupffer cell binding through N-acetylgalactosamine-specific C-type lectin-like receptors is crucial for DC recruitment to the liver. Rat DCs at least partly possess receptors for endocytosis of galactosylated antigens. These DC receptors as well as Kupffer cell lectins are presumably responsible for this binding.

Acetylgalactosamine↗
PubMed2001

Human CC chemokine liver-expressed chemokine/CCL16 is a functional ligand for CCR1, CCR2 and CCR5, and constitutively expressed by hepatocytes.

Liver-expressed chemokine (LEC)/CCL16 is a human CC chemokine selectively expressed in the liver. Here, we investigated its receptor usage by calcium mobilization and chemotactic assays using mouse L1.2 pre-B cell lines stably expressing a panel of 12 human chemokine receptors. At relatively high concentrations, LEC induced calcium mobilization and chemotaxis via CCR1 and CCR2. LEC also induced calcium mobilization, but marginal chemotaxis via CCR5. Consistently, LEC was found to bind to CCR1, CCR2 and CCR5 with relatively low affinities. The binding of LEC to CCR8 was much less significant. In spite of its binding to CCR5, LEC was unable to inhibit infection of an R5-type HIV-1 to activated human peripheral blood mononuclear cells even at high concentrations. In human liver sections, hepatocytes were strongly stained by anti-LEC antibody. HepG2, a human hepatocarcinoma cell line, was found to constitutively express LEC. LEC was also present in the plasma samples from healthy adult donors at relatively high concentrations (0.3--4 nM). Taken together, LEC is a new low-affinity functional ligand for CCR1, CCR2 and CCR5, and is constitutively expressed by liver parenchymal cells. The presence of LEC in normal plasma at relatively high concentrations may modulate inflammatory responses.

Animals↗
PubMed2001

Detection of myocardial viability using rest-redistribution thallium-201 imaging in a stress 99Tcm-tetrofosmin/rest thallium-201 dual-isotope protocol.

This study investigated the utility of optional thallium-201 (201Tl) imaging for detecting myocardial viability in the stress 99Tcm-tetrofosmin/rest 201Tl dual-isotope protocol. Seventy-nine patients with old myocardial infarction and 25 patients with acute myocardial infarction underwent acquisition of three consecutive 201Tl images (early, intermediate and delayed) using the dual-isotope protocol. A polar map was created and defect scores (extent and severity) were determined by comparison with normal control data. Fluorodeoxyglucose positron emission tomography was also performed in 16 patients with old myocardial infarction. In patients with old infarction, the severity score decreased significantly from the early to the intermediate images, and decreased further on the delayed images. In patients with acute infarction, the score increased from the early to the intermediate images, but not on the delayed images. Regional uptake on the delayed images showed a better correlation with the fluorodeoxyglucose images than that on the early images. Redistribution on the delayed images was exclusively observed in the myocardial segments with less uptake than that estimated by fluorodeoxyglucose. In conclusion, addition of delayed 201Tl imaging to the dual-isotope protocol could improve the sensitivity for detecting myocardial viability.

Aged↗
PubMed2001

A human protein with sequence similarity to Drosophila mastermind coordinates the nuclear form of notch and a CSL protein to build a transcriptional activator complex on target promoters.

Mastermind (Mam) has been implicated as an important positive regulator of the Notch signaling pathway by genetic studies using Drosophila melanogaster. Here we describe a biochemical mechanism of action of Mam within the Notch signaling pathway. Expression of a human sequence related to Drosophila Mam (hMam-1) in mammalian cells augments induction of Hairy Enhancer of split (HES) promoters by Notch signaling. hMam-1 stabilizes and participates in the DNA binding complex of the intracellular domain of human Notch1 and a CSL protein. Truncated versions of hMam-1 that can maintain an association with the complex behave in a dominant negative fashion and depress transactivation. Furthermore, Drosophila Mam forms a similar complex with the intracellular domain of Drosophila Notch and Drosophila CSL protein during activation of Enhancer of split, the Drosophila counterpart of HES. These results indicate that Mam is an essential component of the transcriptional apparatus of Notch signaling.

Amino Acid Sequence↗