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Biomedical subjects

Makoto Inoue

Publications and source records attributed to Makoto Inoue.

At least 73 records · Page 4Linked to original sources
PubMed2005

The herbal medicine Sho-saiko-to selectively inhibits CD8+ T-cell proliferation.

Sho-saiko-to (SST), a Chinese/Japanese traditional herbal medicine, has been widely used to treat chronic hepatitis in Japan, and the immunomodulatory properties of SST are likely to mediate its beneficial effect. In the present study, we examined the effects of SST and its various ingredients on the count and proliferation of T-cell subsets in cultured splenocytes and hepatic mononuclear cells. SST, wogonin-7-O-glucuronoside (a major SST ingredient), and wogonin (an intestinal metabolite of wogonin-7-O-glucuronoside) increased CD4/CD8 ratio via a decrease of CD8+ T-cell counts with no effect on CD4+ T-cell counts. Flow cytometric analyses of viability, proliferation, and cell cycle revealed that wogonin suppressed CD8+ T-cell proliferation without inducing cell death. SST and wogonin administered to mice increased the CD4/CD8 ratio in hepatic mononuclear cells but not in splenocytes. These findings suggest that SST may modulate the CD4/CD8 ratio via the selective inhibition of CD8+ T-cell proliferation by the SST ingredient wogonin-7-O-glucuronoside or its metabolite wogonin.

Animals↗
PubMed2005

Intraocular lens implantation after atopic cataract surgery decreases incidence of postoperative retinal detachment.

PURPOSE: To investigate the efficacy of intraocular lens (IOL) implantation in reducing the incidence of postoperative retinal detachment after cataract surgery in patients with atopic dermatitis. DESIGN: Retrospective review. PARTICIPANTS: One hundred sixty-nine eyes of 126 patients who underwent cataract surgery for atopic cataract were followed for more than 1 year. None of the eyes previously had a retinal detachment or retinal detachment surgery. METHODS: The eyes were divided into 132 eyes of 95 patients with an IOL implantation (IOL group) and 37 eyes of 31 patients without an IOL implantation (aphakia group). The postoperative visual acuity and incidence of postoperative retinal detachment were compared between the 2 groups. The effects of the location of the causative retinal breaks, intraoperative posterior capsule rupture, and postoperative posterior capsulotomy on the incidence of retinal detachments were evaluated. MAIN OUTCOME MEASURES: The postoperative corrected visual acuity, incidence of postoperative retinal detachment, and influence of intraoperative posterior capsule rupture on the retinal detachment. RESULTS: The final visual acuity was better than or equal to 20/20 in 128 eyes (97.0%) of the IOL group and in 29 eyes (78.4%) of the aphakia group (P = 0.0007). Retinal detachment after an uncomplicated cataract surgery occurred in 3 eyes (2.3%) of the IOL group and in 8 eyes (25.8%) of the aphakia group (P<0.0001, Mantel-Cox). Two of 3 eyes (66.7%) in the IOL group and 1 of 8 eyes (16.7%) in the aphakia group that later developed a retinal detachment had an intraoperative posterior capsule rupture. Posterior capsulotomy by yttrium-aluminum-garnet laser did not seem to alter the incidence of postoperative retinal detachment in either the IOL (2.0%) or the aphakia group (25.0%). CONCLUSIONS: The rate of postoperative retinal detachment in eyes with IOL and no intraoperative posterior capsule rupture seems to be low. Intraocular lens implantation with capsular bag fixation may reduce the incidence of postoperative retinal detachment triggered by lens surgery for atopic cataract.

Adolescent↗
PubMed2005

AIP1/Alix is a binding partner of Sendai virus C protein and facilitates virus budding.

The C protein, an accessory protein of Sendai virus (SeV), has anti-interferon capacity and suppresses viral RNA synthesis. In addition, it is thought that the C protein is involved in virus budding because of the low efficiency of release of progeny virions from C-knockout virus-infected cells and because of the requirement of the C protein for efficient release of virus-like particles. Here, we identified AIP1/Alix, a host protein involved in apoptosis and endosomal membrane trafficking, as an interacting partner of the C protein using a yeast two-hybrid system. The amino terminus of AIP1/Alix and the carboxyl terminus of the C protein are important for the interaction in mammalian cells. Mutant C proteins unable to bind AIP1/Alix failed to accelerate the release of virus-like particles from cells. Furthermore, overexpression of AIP1/Alix enhanced SeV budding from infected cells in a C-protein-dependent manner, while the release of nucleocapsid-free empty virions was also enhanced. Finally, AIP1/Alix depletion by small interfering RNA resulted in suppression of SeV budding. The results of this study suggest that AIP1/Alix plays a role in efficient SeV budding and that the SeV C protein facilitates virus budding through interaction with AIP1/Alix.

ATPases Associated with Diverse Cellular Activitie↗
PubMed2005

Selective suppression of pathologic, but not physiologic, retinal neovascularization by blocking the angiotensin II type 1 receptor.

PURPOSE: To investigate the anti-inflammatory and anti-angiogenic effects of telmisartan, an angiotensin II type 1 receptor (AT1-R) antagonist, on ischemia-induced retinal neovascularization. METHODS: C57BL/6 neonatal mice were reared in an 80% concentration of oxygen from postnatal day (P)7 to P12, followed by room-air breathing until P17, to induce ischemia-initiated retinal neovascularization (i.e., a murine model of ischemic retinopathy). Tissue localization of AT1-R was examined by immunohistochemistry for murine retinal wholemounts and human fibrovascular tissues excised at vitrectomy for proliferative diabetic retinopathy. Animals received intraperitoneal injection of telmisartan or vehicle. A concanavalin A lectin perfusion-labeling technique was used to evaluate the areas of physiological and pathologic retinal new vessels and the number of leukocytes adhering to the vasculature. Retinal mRNA and protein levels of intercellular adhesion molecule (ICAM)-1, vascular endothelial growth factor receptor (VEGFR)-1, and VEGFR-2 were examined by RT-PCR and ELISA. RESULTS: Vessels in human fibrovascular tissues and the murine retinas were positive for AT1-R. Pathologic (P < 0.01), but not physiologic (P > 0.05), retinal neovascularization was significantly suppressed in telmisartan-treated mice compared with vehicle-treated animals. The number of adherent leukocytes (P < 0.01) was also significantly reduced, together with retinal ICAM-1 levels (P < 0.01) in the telmisartan-treated group compared with the control group. No significant difference was detected in retinal VEGFR-2 levels between the two groups, whereas retinal VEGFR-1 levels in the telmisartan-treated group were significantly (P < 0.05) lower than in the vehicle-treated group. CONCLUSIONS: The present findings suggest that the AT1-R signaling blockade leads to the selective suppression of pathologic, but not physiological, retinal neovascularization through the inhibition of the inflammatory processes related to pathologic neovascularization.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2005

Suppression of ocular inflammation in endotoxin-induced uveitis by blocking the angiotensin II type 1 receptor.

PURPOSE: To examine whether the angiotensin II type 1 receptor (AT1-R) signaling plays a role in ocular inflammation in endotoxin-induced uveitis (EIU). METHODS: EIU was induced in C57BL/6 mice by a single intraperitoneal injection of 150 mug lipopolysaccharide (LPS). Tissue localization, mRNA expression, and protein levels of AT1-R in murine retinas were examined by immunohistochemistry, RT-PCR, and Western blot analyses, respectively. Telmisartan, an AT1-R antagonist widely used as an antihypertensive agent, was administered intraperitoneally at a dose of 10 mg/kg daily for 5 days until the injection of LPS. Twenty-four hours after administration, leukocyte adhesion to the retinal vasculature was evaluated with a concanavalin A lectin perfusion-labeling technique. Retinal mRNA and protein levels of intercellular adhesion molecule (ICAM)-1 were examined by RT-PCR and ELISA, respectively. Protein concentration and inflammatory cells in the aqueous humor were also measured. RESULTS: Retinal vessels were positive for AT1-R. In mice with EIU, retinal AT1-R mRNA and protein levels were significantly increased when compared to the normal control. EIU animals also showed significant increases in the number of inflammatory cells infiltrating the anterior chamber and adhering to the retinal vessels and in retinal ICAM-1 levels. Administration of telmisartan to EIU mice resulted in significant suppression of retinal ICAM-1 expression and leukocyte adhesion and infiltration compared with vehicle treatment. Protein concentration in the aqueous humor of telmisartan-treated EIU mice tended to be lower than that of vehicle-treated EIU mice, but the difference was not statistically significant. CONCLUSIONS: AT1-R signaling blockade inhibited retinal ICAM-1 upregulation and leukocyte adhesion and infiltration in the EIU model. These results suggest the potential use of an AT1-R antagonist as a therapeutic agent to reduce ocular inflammation.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2005

pX gene causes hypercholesterolemia in hypercholesterolemia-resistant BALB/c mice.

To investigate the high incidence of atherosclerosis in the patients affected with rheumatoid arthritis, we examined the effect of feeding a cholesterol-enriched diet on the development of hypercholesterolemia in pX transgenic mice, which spontaneously develop chronic inflammatory arthritis. Cholesterol feeding to pX transgenic mice induced a striking elevation in serum total cholesterol (ca. 500 mg/dl) compared with their littermates, BALB/c mice used as controls. The pX transgenic mice exhibited elevated mRNA levels of ACAT1, and ABCG5 in the small intestine compared with their littermates, and furthermore, apoA1, ABCA1, ABCG5, ACAT1, and ACAT2 mRNAs were induced more easily by a cholesterol-enriched diet in pX transgenic mice than their littermates. As ACAT1 mRNA in the small intestine is known not to be induced by feeding a cholesterol-enriched diet, a possibility was inferred that interferon-gamma induced by Tax, a pX gene product, might play an important role in the induction of ACAT1 mRNA and the following hypercholesterolemia. These findings suggest that pX gene plays an important role in inducing hypercholesterolemia in BALB/c mice, which are genetically less susceptible to hypercholesterolemia and atherosclerosis and that RA patients carrying HTLV-1 virus have a predilection for hypercholesterolemia, a main risk factor for cardiovascular diseases.

Animals↗
PubMed2005

Sendai virus for gene therapy and vaccination.

Sendai virus (SeV), also known as hemagglutinating virus of Japan (HVJ), is a negative-strand RNA virus and a member of the paramyxovirus family. The capacity of SeV to enhance fusion of lipid vesicles and cell membranes was recognized in the early 1980s, and has since been utilized in the form of HVJ-liposomes. More recently, advances in reverse genetics have allowed the construction of a new class of RNA vector with cytoplasmic expression, namely non-transmissible recombinant SeV. Extensive preclinical studies have shown the therapeutic potential of this vector for use in airways, brain and for ischemic diseases and tumors. In addition, the potential of SeV vector for vaccination has been explored. Data on the use of SeV for gene therapy and vaccination since January 2004 are reviewed and recent improvements in SeV vectorology are discussed.

AIDS Vaccines↗
PubMed2004

Prevention of nanoparticle coalescence under high-temperature annealing.

An effective method of employing 3-aminopropyldimethylethoxysilane linker molecules to stabilize 4.4 nm FePt nanoparticle monolayer films on a SiO2 substrate as well as to prevent coalescence of the particles under 800 degrees C annealing is reported. As-deposited FePt nanoparticle films in chemically disordered face-centered-cubic phase transform to mostly chemically ordered L1 0 structure after annealing, while the nanoparticles are free from serious coalescence. The method may fulfill the pressing need to prevent nanoparticle coalescence under high-temperature annealing for the development of FePt nanoparticle based products, such as ultrahigh-density magnetic recording media and novel memory devices.

Journal Article↗
PubMed2004

Solution structure of the rhodanese homology domain At4g01050(175-295) from Arabidopsis thaliana.

The three-dimensional structure of the rhodanese homology domain At4g01050(175-195) from Arabidopsis thaliana has been determined by solution nuclear magnetic resonance methods based on 3043 upper distance limits derived from NOE intensities measured in three-dimensional NOESY spectra. The structure shows a backbone root mean square deviation to the mean coordinates of 0.43 A for the structured residues 7-125. The fold consists of a central parallel beta-sheet with five strands in the order 1-5-4-2-3 and arranged in the conventional counterclockwise twist, and helices packing against each side of the beta-sheet. Comparison with the sequences of other proteins with a rhodanese homology domain in Arabidopsis thaliana indicated residues that could play an important role in the scaffold of the rhodanese homology domain. Finally, a three-dimensional structure comparison of the present noncatalytic rhodanese homology domain with the noncatalytic rhodanese domains of sulfurtransferases from other organisms discloses differences in the length and conformation of loops that could throw light on the role of the noncatalytic rhodanese domain in sulfurtransferases.

Amino Acid Sequence↗
PubMed2004

Solution structure of the B3 DNA binding domain of the Arabidopsis cold-responsive transcription factor RAV1.

The B3 DNA binding domain is shared amongst various plant-specific transcription factors, including factors involved in auxin-regulated and abscisic acid-regulated transcription. Herein, we report the NMR solution structure of the B3 domain of the Arabidopsis thaliana cold-responsive transcription factor RAV1. The structure consists of a seven-stranded open beta-barrel and two alpha-helices located at the ends of the barrel and is significantly similar to the structure of the noncatalytic DNA binding domain of the restriction enzyme EcoRII. An NMR titration experiment revealed a DNA recognition interface that enabled us to propose a structural model of the protein-DNA complex. The locations of the DNA-contacting residues are also likely to be similar to those of the EcoRII DNA binding domain.

Acclimatization↗
PubMed2004

Extrinsic tongue and suprahyoid muscle activities during mastication in freely feeding rabbits.

To evaluate the coordination of tongue and suprahyoid muscle activities during natural mastication, electromyograms (EMGs) of jaw-closer, jaw-opener, suprahyoid (mylohyoid, MH), tongue-retractor (styloglossus, SG) and tongue-protractor (genioglossus, GG) muscles were recorded as well as the jaw-movement trajectories in vertical and horizontal axes in awake rabbits. Each masticatory cycle had three components including the fast-closing (FC), slow-closing (SC) and opening (Op) phases. The duration of the SC phase was much longer during pellet chewing while the durations of the FC and Op phases were much shorter during pellet chewing than bread or banana chewing. The jaw movements during banana chewing had a small amplitude of lateral excursion and a large amplitude of gape as compared with those during pellet and bread chewing. The MH muscle exhibited double-peaked EMG bursts during the Op phase. The MH bursts in the late part of the Op phase were dominant on the non-chewing side during pellet and bread chewing. The SG muscle also exhibited double-peaked EMG bursts. During pellet and bread chewing, the SG bursts during the SC phase were significantly larger on the chewing side than the non-chewing side. These bursts were also dominant during pellet chewing as compared with banana chewing. There was little difference in the GG bursts between the chewing and non-chewing sides or among the foods. Our results suggest that patterns of the MH and SG muscle activity are affected by the peripheral inputs and/or chewing patterns while those of the GG muscle activity was less modulated regardless of the consistency of foods.

Animal Feed↗
PubMed2004

Effects of food consistency on the pattern of extrinsic tongue muscle activities during mastication in freely moving rabbits.

The effects of physical characteristics of foods on the coordination of extrinsic tongue muscle activities during natural mastication were evaluated. Electromyograms of tongue-retractor (styloglossus, SG) and tongue-protractor (genioglossus, GG) muscles as well as the jaw-movement trajectories were recorded during raw rice and chow pellet chewing in the freely moving rabbit. Each masticatory cycle included a jaw closing (Cl) phase consisting of a fast-closing (FC) and a slow-closing (SC) phase, and a jaw opening (Op) phase. The duration of the Cl and SC phases was found to be much larger while the duration of the FC phase was much smaller during rice chewing than pellet chewing. The jaw movements during rice chewing had smaller amplitudes of the gape and lateral excursion of the jaw as compared with those during pellet chewing. The SG muscle had a double-peaked burst activity in each masticatory cycle with one peak during the Op phase (the SG1 burst) and the other during the Cl phase (the SG2 burst). They were significantly larger during pellet chewing as compared with rice chewing, but the duration of the SG2 burst was significantly longer during rice chewing than pellet chewing. The offset of the SG2 burst was delayed during rice chewing as compared with that during pellet chewing. There was little difference in the activity pattern of the GG burst between the foods. Our present results suggest that the SG muscle activity could be modified by the sensory feedback possibly to adapt to environmental demands during chewing.

Animals↗
PubMed2004

Partitioning of NaPi cotransporter in cholesterol-, sphingomyelin-, and glycosphingolipid-enriched membrane domains modulates NaPi protein diffusion, clustering, and activity.

In dietary potassium deficiency there is a decrease in the transport activity of the type IIa sodium/phosphate cotransporter protein (NaPi) despite an increase in its apical membrane abundance. This novel posttranslational regulation of NaPi activity is mediated by the increased glycosphingolipid content of the potassium-deficient apical membrane. However, the mechanisms by which these lipids modulate NaPi activity have not been determined. We determined if in potassium deficiency NaPi is increasingly partitioned in cholesterol-, sphingomyelin-, and glycosphingolipid-enriched microdomains of the apical membrane and if the increased presence of NaPi in these microdomains modulates its activity. By using a detergent-free density gradient flotation technique, we found that 80% of the apical membrane NaPi partitions into the low density cholesterol-, sphingomyelin-, and GM1-enriched fractions characterized as "lipid raft" fractions. In potassium deficiency, a higher proportion of NaPi was localized in the lipid raft fractions. By combining fluorescence correlation spectroscopy and photon counting histogram methods for control and potassium-deficient apical membranes reconstituted into giant unilamellar vesicles, we showed a 2-fold decrease in lateral diffusion of NaPi protein and a greater than 2-fold increase in size of protein aggregates/clusters in potassium deficiency. Our results indicate that NaPi protein is localized in membrane microdomains, that in potassium deficiency a larger proportion of NaPi protein is present in these microdomains, and that NaPi lateral diffusion is slowed down and NaPi aggregation/clustering is increased in potassium deficiency, both of which could be associated with the decreased Na/Pi cotransport activity in potassium deficiency.

Animals↗
PubMed2004

Coordination of jaw and extrinsic tongue muscle activity during rhythmic jaw movements in anesthetized rabbits.

To clarify the jaw-closer and tongue-retractor muscle activity patterns during mastication, electromyographic activity of the styloglossus (SG) as a tongue-retractor and masseter (Mass) as a jaw-closer muscles as well as jaw-movement trajectories were recorded during cortically evoked rhythmic jaw movements (CRJMs) in anesthetized rabbits. The SG and Mass muscles were mainly active during the jaw-closing (Cl) phase. The SG activity was composed of two bursts in one masticatory cycle; one had its peak during the jaw-opening (Op) phase (SG1 burst) and the other during the Cl phase (SG2 burst). The Mass activity during the Cl phase was dominant on the working side (opposite to the stimulating side) while the SG1 and SG2 bursts were not different between the sides. When the wooden stick was inserted between the molar teeth on the working side during CRJMs, the facilitatory effects on the SG1 and SG2 bursts on both sides were noted as well as those on the Mass bursts, but the effects on the SG1 burst seemed to be weak as compared with those on the Mass and SG2 bursts. The difference in the burst timing between the sides was noted only in the SG1 burst. When the trigeminal nerves were blocked, the peak and area of the SG and Mass burst decreased during CRJMs, and the facilitatory effects of the wooden stick application on the muscles were not noted. The results suggest that the jaw and tongue muscle activities may be adjusted to chew the food and make the food bolus.

Anesthesia↗
PubMed2004

The Sprouty-related protein, Spred, inhibits cell motility, metastasis, and Rho-mediated actin reorganization.

Sprouty and the Sprouty-related protein, Spred (Sprouty-related Ena/vasodilator-stimulated phosphoprotein homology-1 (EVH1) domain-containing protein), inhibit Ras-dependent extracellular signal-regulated kinase (ERK) signaling induced by a variety of growth factors. Since Sprouty proteins have been shown to inhibit not only ERK activation but also cell migration, we postulated that Spreds also inhibit cellular migration. Using stably highly metastatic LM8 cells infected with the Spred1-Sendai virus vector, we demonstrated that Spred1 inhibits the metastasis of LM8 cells in nude mice. Spred1 overexpression also inhibited migration of cells in vitro in response to chemokines, CCL19 and CCL21. We also found that Spred1 overexpression dissolved actin-stress fibers. Both EVH1 domain and C-terminal Sprouty-related domain were required for actin reassembly. Spred1 and Spred2 suppressed constitutively activated RhoA (V14RhoA)-induced stress fiber formation and serum response factor activation. Spred1 bound to activated RhoA, but not cdc42 and Rac. Spred1 also inhibited chemokine-induced RhoA activation and active RhoA-induced Rho-kinase activation. These data suggest that Spreds are key regulators of RhoA-mediated cell motility and signal transduction. Furthermore, our study suggests that the induction of Spreds could be a novel strategy for preventing cancer cell metastasis.

Actins↗
PubMed2004

Initiation of neuropathic pain requires lysophosphatidic acid receptor signaling.

Lysophosphatidic acid (LPA) is a bioactive lipid with activity in the nervous system mediated by G-protein-coupled receptors. Here, we examined the role of LPA signaling in the development of neuropathic pain by pharmacological and genetic approaches, including the use of mice lacking the LPA(1) receptor. Wild-type animals with nerve injury develop behavioral allodynia and hyperalgesia paralleled by demyelination in the dorsal root and increased expression of both the protein kinase C gamma-isoform within the spinal cord dorsal horn and the alpha(2)delta(1) calcium channel subunit in dorsal root ganglia. Intrathecal injection of LPA induced behavioral, morphological and biochemical changes similar to those observed after nerve ligation. In contrast, mice lacking a single LPA receptor (LPA(1), also known as EDG2) that activates the Rho-Rho kinase pathway do not develop signs of neuropathic pain after peripheral nerve injury. Inhibitors of Rho and Rho kinase also prevented these signs of neuropathic pain. These results imply that receptor-mediated LPA signaling is crucial in the initiation of neuropathic pain.

ADP Ribose Transferases↗