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Biomedical subjects

M Noda

Publications and source records attributed to M Noda.

At least 397 records · Page 22Linked to original sources
PubMed1994

Expression of platelet membrane glycoprotein V in human megakaryocytes and megakaryocytic cell lines: a study using a novel monoclonal antibody against GPV.

Glycoprotein V (GPV) is a platelet membrane protein with a molecular weight of 82 kD, and one of the leucine rich glycoproteins (LRG). By reverse transcription-polymerase chain reaction (RT-PCR), GPV cDNA was amplified from mRNA of platelets and megakaryocytic cell lines. However, since there are few reports indicating whether GPV protein is expressed in megakaryocytes as a lineage and maturation specific protein, we studied the GPV expression at the protein level by using a novel monoclonal antibody (1D9) recognizing GPV. Flow cytometric and immunohistochemical analysis indicated that GPV was detected on the surface and in the cytoplasm of only the megakaryocytes in bone marrow aspirates. In a megakaryocytic cell line UT-7, GPV antigen increased after treatment with phorbol-12-myristate-13-acetate (PMA). These data indicate that only megakaryocytes specifically express the GPV protein among hematopoietic cells and that the expression of GPV increases with differentiation of the megakaryocyte as GPIb-IX complex.

Antibodies, Monoclonal↗
PubMed1994

[Effect of amurinone on human pulmonary artery in vitro].

We studied the effect of amurinone, a phosphodiesterase inhibitor, on human pulmonary arterial smooth muscle in vitro. Amurinone caused dose-dependent relaxation of pulmonary arterial strips precontracted with 60 mM KCl. Preincubation with either meclofenamate (31 microM), a cyclooxygenase inhibitor, or L-NG-nitroarginine (100 microM), an endothelium-derived relaxing factor (EDRF) production inhibitor, failed to inhibit amurinone-induced pulmonary vasodilation. The cyclic AMP (cAMP) levels in the supernatant of the lung vessel homogenates significantly increased after incubation with amurinone. These results indicate that amurinone causes relaxation of human pulmonary artery in vitro, and suggest a role for cAMP in the mechanisms of amurinone-induced pulmonary vasodilation.

Adult↗
PubMed1994

[A pedigree with maternally transmitted diabetes mellitus, deafness and cardiomyopathy].

A pedigree with maternally transmitted diabetes mellitus, deafness, and cardiomyopathy is described. A A-->G mutation at nucleotide pair 3243 in mitochondrial gene was detected by Apa I digestion of PCR amplified genomic DNA from 3 brothers and their mother. The proband, suffering from CHF, showed unique fine granular pattern of hyperechogenic cardiomyopathy as his brother and their mother did. Although he is recently treated with insulin, he was initially NIDDM treated by sulfonylurea. His urinary CPR excretion decreased gradually to as low as less than 10 micrograms/day in these 3 years. The insulin response to oral glucose was decreased in all other family members with the mutation. It is suggested that the defective insulin secretion exists in this family with the mutation and the progressive decrease in insulin secretion might resulted in IDDM in the proband.

Adult↗
PubMed1994

[Lung 3H-thymidine incorporation in monocrotaline (MCT)-treated rats--role of platelet-activating factor (PAF)].

Monocrotaline (MCT) causes chronic pulmonary hypertension associated with pulmonary vascular thickening in rats. Since components of the pulmonary vascular thickening are reflected in increased DNA synthesis in medial smooth muscle cells, and since platelet-activating factor (PAF) has been reported to contribute to the pulmonary hypertension induced by MCT, we examined the effect of WEB 2170, a specific PAF receptor blocker, on MCT-induced pulmonary vascular thickening and in vitro 3H-thymidine incorporation into lung tissue, as an index of stimulation of cell proliferation. In MCT-treated rats, pulmonary hypertension, right ventricular hypertrophy, and pulmonary vascular thickening developed at 3 weeks after injection. Also, in MCT-treated rat lung tissue, there was a significant increase in the in vitro 3H-thymidine incorporation rate. In WEB 2170-treated MCT rats, these changes were significantly less severe than those observed in rats receiving MCT alone. We conclude that PAF plays a role in the inflammatory process that contributes to the development of pulmonary hypertension and vascular remodeling associated with increased lung cell proliferation in MCT-treated rats.

Animals↗
PubMed1994

Erythropoietin receptor and interleukin-2 receptor use different downstream signaling pathways for proliferation and apoptosis-block.

Erythropoietin (EPO) regulates proliferation and differentiation and prevents apoptosis of erythroid progenitor cells by binding to erythropoietin receptor (EPOR) expressed on the surface of those cells. The mechanism by which EPO signal is transmitted to the cells through EPOR is still unclear. In the present study, we introduced and expressed EPOR in an interleukin-3 (IL-3) dependent pro-B cell line, BAF-B03 and an interleukin-2 (IL-2)-dependent cytotoxic T cell line, CTLL-2 and analyzed their growth response to EPO and the DNA breakdown characteristic to apoptosis after deprivation of the growth factor. BAF-B03-derived cells expressing EPOR proliferated in response to EPO but CTLL-2-derived cells expressing EPOR (C/EPOR) did not. DNA from C/EPOR cells cultured in the absence of IL-2 with or without EPO had similar patterns of DNA breakdown. These results suggest that downstream signaling pathways for the cell proliferation and apoptosis-block are, at least, partially different between EPOR and IL-2 receptor (IL-2R).

Animals↗
PubMed1993

[Radiotherapy for symptomatic osseous metastases: special reference to the analysis of patients achieved complete pain relief].

A total of 223 patients with 498 symptomatic osseous metastases treated by radiotherapy between July 1985 and June 1991 were retrospectively analyzed. Most sites, 409 (82%), were irradiated by conventional fractionation, while the remaining 89 sites were irradiated by dose-increment fractionation, low-dose short schedules or hyperfractionation. The total dose ranged from 5.4 to 74 Gy (mean, 41.4 Gy). Daily pain assessment was done by patients themselves on an 11-point scale, i.e., 10: pretreatment pain, 0: disappearance of pain following radiotherapy. In addition, improvement in performance status (PS) and the duration of complete pain relief were assessed. The following results were obtained. 1) Pain relief: Of 498 evaluated sites, complete pain relief and partial pain relief were achieved in 403 sites (81%) and 64 sites (13%), respectively. No significant difference was seen in the incidence of complete pain relief between weight-bearing bone and non-weight-bearing bone. Patients with PS 1, 2 or 3 were significantly superior to those with PS 4 in terms of complete pain relief (P < 0.05-0.001). The complete response rate increased in accordance with the dose delivered, i.e., 49% at 20 Gy, 70% at 30 Gy and 77% at 40 Gy, in all of the 498 sites irradiated; 60%, 86% and 95% of 403 sites, respectively, achieved complete pain relief. Regarding the fractionation regimens, dose-increment fractionation was superior to both conventional fractionation and low-dose short schedules in terms of complete pain relief rate. 2) Improvement of PS: Of 223 evaluated patients, PS was improved 1 to 3 steps in 162 (73%) at the completion of radiotherapy. The improvement rates of patients with PS 2 or 3 were significantly better than those with PS 4 (P < 0.025, 0.001). 3) Duration of complete pain relief: Of 288 appraisable sites, the recurrence of pain was recognized in 23 (9%) at intervals of 3 to 21 months (median, 5 months). On the other hand, the duration of pain relief was 16 to 79 months (median, 32 months) in 26 sites of survivors, and 1 to 28 months (median, 5 months) in 239 sites of decreased patients. The mean total dose was 48.5 Gy (TDF: 82) to 62 sites with a duration of pain relief of more than 13 months. 4) Re-irradiation to the same site: Of 14 sites retreated after initial complete response with a total dose of 30 to 50 Gy (mean, 48 Gy), 11 (79%) were in weight-bearing bone and 9 (64%) responded completely. 5) Patients with unsatisfactory pain relief (pain score > or = 6): Of 31 sites, 27 (94%) were in patients with PS 4, and 19 (61%) received a total dose below 30 Gy. 6) The 11-point scale for patient self-assessment of pain relief following radiotherapy was thought to be useful and easy to adopt in general clinics.

Adolescent↗
PubMed1993

Stationary phase-specific expression of the fic gene in Escherichia coli K-12 is controlled by the rpoS gene product (sigma 38).

The fic gene, near pabA located at 75 min of the Escherichia coli chromosome, was previously identified as the regulatory factor of cell division. In this paper we have examined how fic gene expression is controlled during the growth cycle using a fic-lacZ protein fusion plasmid (pFL1). Its expression was induced at stationary phase while it was nearly abolished in rpoSmutants. Using a RNase protection assay, fic transcript at stationary phase was detected in rpoS+ strains, but not in the rpoS mutants. Furthermore, primer extension analysis indicated that the fic transcript controlled by RpoS initiates at a G located 185 bp upstream from ATG of the fic coding region. Compared with the sigma 70 recognition sequence, the -10 region of fic promoter resembled the Pribnow box, but no homologous sequence was observed at the -35 region. These results were consistent with the characteristic sequence profile of fic promoter recognized specifically by RpoS in vitro, which is the only example of the type III promoter so far detected in vitro and in vivo.

Bacterial Proteins↗
PubMed1993

Purification of chondroitin 6-sulfotransferase secreted from cultured chick embryo chondrocytes.

Chondroitin 6-sulfotransferase, which transfers sulfate from 3'-phosphoadenylyl sulfate to position 6 of N-acetylgalactosamine in chondroitin, was purified 1,430-fold to apparent homogeneity with a 22% yield from the serum-free culture medium of chick embryo chondrocytes by affinity chromatography on heparin-Sepharose CL-6B, wheat germ agglutinin-agarose, and 3',5'-ADP-agarose. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the purified enzyme showed a single broad protein band with an apparent molecular weight of 75,000. Since the purified enzyme has an apparent molecular weight of 160,000 as judged by gel chromatography on Superose 12, the active form of chondroitin 6-sulfotransferase may be a dimer. The purified enzyme transferred sulfate to chondroitin, chondroitin sulfate, and corneal keratan sulfate. Chondroitin sulfate E from squid cartilage, dermatan, sulfate, and heparan sulfate hardly served as acceptors of the sulfotransferase. The sulfated product derived from keratan sulfate was degraded by keratanase but not by chondroitinase ABC.

Animals↗
PubMed1993

Bone morphogenetic protein 2 transiently enhances expression of a gene, Id (inhibitor of differentiation), encoding a helix-loop-helix molecule in osteoblast-like cells.

Bone morphogenetic protein 2 (BMP-2) is a potent inducer of differentiation of osteoblasts both in vivo and in vitro. We examined the action of BMP-2 on expression of a helix-loop-helix-type transcription factor, Id (inhibitor of differentiation), in osteoblast-like cells, as well as in osteoblast-enriched cells and possible precursor cells. To our surprise, BMP-2 enhanced Id gene expression in the cell types of osteoblastic lineage we examined. The maximal BMP-2 enhancement was observed within 24 hr in early proliferating cultures and the enhancement lasted up to 96 hr. The BMP-2 effect was not blocked by actinomycin D, while it was blocked by cycloheximide, suggesting that BMP-2 regulates Id gene expression at least in part via posttranscriptional events, which require protein synthesis. Other experiments indicated that BMP-2 did not further enhance Id mRNA levels promoted by dexamethasone, while BMP-2 did not resume the Id mRNA levels suppressed by 1,25-dihydroxyvitamin D3. Similar BMP-2 enhancement of Id message expression was also observed in osteoblast-enriched fetal rat calvaria cells as well as C3H10T1/2 cells. These results indicate that BMP-2 enhances expression of Id in early cultures of osteoblastic cells and suggest that enhancement of Id expression may somehow be involved in the promotion of differentiation by this cytokine in these osteoblastic cells and in their precursor cells.

3T3 Cells↗
PubMed1993

Cloning of a cDNA which encodes a novel ubiquitin-like protein.

The cloning of a mouse cDNA, Nedd-8, which encodes a small novel protein of 81 amino acid residues with a relative molecular mass of 9 kDa, is described. The putative Nedd-8 product is approximately 60% identical to ubiquitin protein. The 0.6 kb mRNA for Nedd-8 gene can be detected in various mouse tissues and cell lines derived from various sources. Nedd-8 probe hybridizes to genomic DNA from various vertebrate species as well as yeast, indicating high degree of interspecies conservation. These data suggest that like ubiquitin, the product of this gene may play some essential role in eukaryotic cellular metabolism.

Amino Acid Sequence↗
PubMed1993

Inhibition of rabbit aortic angiotensin II (AII) receptor by CV-11974, a new nonpeptide AII antagonist.

The angiotensin II (AII) antagonistic action of CV-11974 (2-ethoxy-1-[[2'-(1H-tetrazol-5-yl)biphenyl-4-yl]methyl] benzimidazole-7-carboxylic acid) was investigated in an AII-receptor binding assay using rabbit aortic membranes and an AII-induced contraction assay using rabbit aortic strips. A single class of [125I]AII-(Sar1,Ile8) binding sites was found in the membranes with a dissociation constant (Kd) of 0.15 nM and a receptor concentration (Bmax) of 86.9 fmol/mg protein. CV-11974 markedly reduced Kd without affecting Bmax. The specific binding of [125I]AII-(Sar1,Ile8) in this preparation was inhibited completely by CV-11974 [the inhibition constant (Ki) = 0.64 nM], DuP 753 [an angiotensin II type I (AT1) receptor-selective antagonist] (Ki = 51 nM) and EXP3174 (an active metabolite of DuP 753) (Ki = 6.8 nM), but was not affected by PD123177 (an AT2 receptor-selective antagonist). These results suggest that the single binding site in rabbit aortic membranes is an AT1 receptor subtype. The affinity of CV-11974 to these AT1 receptors was approximately 80 and 10 times higher than that of DuP 753 and EXP3174, respectively. CV-11974 showed no appreciable affinity for the AT2 receptors found in bovine cerebellum. In the in vitro functional study, CV-11974 markedly reduced the AII-induced maximal contractile response of rabbit aortic strips (pD'2 = 9.97). In contrast, Compound 7-H, which lacks the carboxyl group at the benzimidazole ring of CV-11974, inhibited the contraction in a competitive manner. The inhibition by CV-11974 was long lasting. These results suggest that CV-11974 is a potent and long-acting AT1 receptor-selective, competitive antagonist. The carboxyl group at the benzimidazole ring plays an important role in the interaction between CV-11974 and the AT1 receptor.

Angiotensin II↗
PubMed1993

Coupling of m2 and m4 muscarinic acetylcholine receptor subtypes to Ca(2+)-dependent K+ channels in transformed NL308 neuroblastoma x fibroblast hybrid cells.

Muscarinic acetylcholine receptor (mAChR) subtype (m1-m4)-specific cDNAs were transfected into NL308 neuroblastoma-fibroblast hybrid cells and clones expressing each of the individual mAChR subtypes m1, m2, m3 and m4 obtained. Acetylcholine increased phosphoinositide (PI) turnover in m1- and m3-transformed cells, but did not produce detectable changes in m2- and m4-transformed cells. In cells expressing m1 and m3 subtypes, ACh produced an initial outward K+ current, followed by a cationic current. In cells expressing m2 and m4 receptors, only the initial K+ current was detected. The outward currents were associated with a rise in intracellular Ca2+ as measured with Fura-2 or Indo-1, and were inhibited by chelating intracellular Ca2+ with external BAPTA-AM, or by external charybdotoxin or Ba2+: hence they were attributed to the activation of a Ca(2+)-dependent K+ current. However, the outward current produced in m2- and m4-transformed cells was blocked by pretreatment with 5 ng ml-1 Pertussis toxin (PTX), whereas that in m1- and m3-transformed cells was not. These results suggest that m2- and m4-receptors in transformed NL308 cells coupled to PTX-sensitive G-protein which is capable of mobilizing intracellular Ca2+ and activate IK(Ca), whereas m1 and m3 receptors activate a similar process through a different, PTX-insensitive G-protein.

Acetylcholine↗