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T Odawara

Publications and source records attributed to T Odawara.

36 records · Page 2Linked to original sources
PubMed1997

Menadione-induced tau dephosphorylation in cultured human neuroblastoma cells.

Oxidative stress has been implicated in the mechanism of aging and neurodegenerative disorders such as Alzheimer's disease (AD). Menadione causes oxidative stress by generating reactive oxygen species through its redox cycling and these free radicals are detoxified subsequently at the expense of intracellular thiol homeostasis. In non-neuronal cells, the cytoskeleton is a prime target of menadione-induced thiol oxidation. We used cultured human neuroblastoma MSN cells in this study to determine how tau proteins in neuronal cells are affected by menadione exposure. Menadione caused a dose-dependent thiol oxidation in these cells just like their non-neuronal counterparts. A prominent consequence of such oxidative insult in these neuronal cells was tau dephosphorylation. This dephosphorylation resulted in disappearance of phosphorylated 57-kDa tau with a concomitant emergence of 53-kDa tau whose full-length nature is indicated by its reactivity with antibodies Alz 50, Tau-1 and Tau-46. Immunochemical analyses using phosphorylation-dependent immunoprobes Tau-1 and PHF-1 with the aid of alkaline phosphatase demonstrated that 53-kDa tau was derived from dephosphorylation of 57-kDa tau. Despite its effect on thiol oxidation, menadione treatment did not lead to cytoskeletal changes reminiscent of the neurofibrillary tangles of AD. The data thus indicate that tau dephosphorylation constitutes a major feature of the menadione-induced oxidative injury in these neuronal cells.

Cell Survival↗
PubMed1997

Host range conversion of murine leukemia virus resulting from recombination with endogenous virus.

Ecotropic murine leukemia viruses (MuLVs) are classified into B-N-, or NB-tropic MuLV by their host range determined by the Fv-1 gene product. B-tropic MuLV is restricted in N-type mouse cells (Fv-1 n/n) and N-tropic MuLV is restricted in B-type mouse cells (FV-1 b/b). Although forced passages in a restrictive host grant a wider host range (NB-tropism), we show here a host range conversion from B to N tropism. The conversion was most likely a result of recombination between the exogenously infected B-tropic MuLV and an endogenously expressed N-tropic MuLV in a C57BL/6 mouse cell line, YH-7.

Animals↗
PubMed1997

One base change is sufficient for host range conversion of murine leukemia virus from B to NB tropism.

Comparison of the whole p30 (CA) sequence between B-tropic WN1802B murine leukemia virus and its NB-tropic derivative revealed a single base change at the 313th nucleotide. We constructed hybrid proviruses differing only at the 313th nucleotide of p30 along the whole genome, and examined the host range of the produced viruses. The single point mutation in p30 was found sufficient for the B to NB tropism conversion.

Animals↗
PubMed1997

Hippocampal pathology in diffuse Lewy body disease using ubiquitin immunohistochemistry.

Various ubiquitin-positive structures in the hippocampus in diffuse Lewy body disease (n=12) and non-demented aged subjects (n=3) were investigated immunohistochemically. These structures were composed of ubiquitin-positive granular structures (UPG), ubiquitin-positive neuritic structures (UPN), spheroidal structures, neuritic plaques, neurofibrillary tangles (NFT), Lewy bodies (LB) and ubiquitin-positive neurons. UPG, UPN, spheroidal structures and neuritic plaques were distributed with special reference to the hippocampal pathway assumed in this study. This pathway was thought to run along the stratum oriens, mostly perforating the stratum pyramidale at many sites of the subiculum and CA1-3, and to end partly in the CA2-3 and the subiculum of the uncus (UPG or UPN). After perforating the stratum pyramidale and giving off terminal branches (ubiquitin-positive neurons or neuritic plaques with degenerative neurites), it was thought to run along the stratum radiatum and continue along the stratum moleculare of the dentate gyrus, forming synapses with the apical dendrites from the stratum pyramidale and the stratum granulosum (spheroidal structures or neuritic plaques). These findings suggest that many of the ubiquitin-positive structures may be caused by degeneration of terminal or distal axons of this pathway. NFT and LB also had a somewhat orderly distribution with reference to this pathway.

Aged↗
PubMed1997

[Parkinsonism in Alzheimer's disease].

Parkinsonism occurs frequently in the patients with Alzheimer type dementia (ATD). The frequency ranges from 9% to 100% of ATD patients, depending on samples, clinical instruments and stages of illness. Several studies have described that rigidity and hypokinesia are the most prevalently observed signs of parkinsonism, and that resting tremor is less. The clinical progress of patients with parkinsonism is more rapid than those of patients without parkinsonism. Patients with parkinsonism are frequently associated with psychiatric symptoms such as depression and delusion. The pathogenesis of parkinsonism in ATD remains to be elucidated, but it should be noted that some cases with parkinsonism correlates with Parkinson's disease pathologic condition, and some have diffuse Lewy body disease.

Alzheimer Disease↗
PubMed1996

Neuropathological evaluation and apolipoprotein E gene polymorphism analysis in diffuse Lewy body disease.

We performed a quantitative neuropathological investigation of senile plaques and neurofibrillary tangles in the brains of 14 Japanese patients with diffuse Lewy body disease (DLBD), and examined apolipoprotein E (APOE) gene polymorphism in these patients. Most DLBD brains had as many senile plaques as those with Alzheimer-type dementia (ATD), but fewer neurofibrillary tangles. The APOE epsilon 4 allele frequency in DLBD was 39.3%, similar to that previously reported in pathologically diagnosed ATD. DLBD and ATD are clinically and pathologically distinct, but may have common mechanisms with regard to the formation of amyloid deposition based on these findings. Future investigation of the pure form of DLBD may clarify the association between Lewy body dementia and APOE.

Aged↗
PubMed1996

Age-related ubiquitin-positive granular structures in non-demented subjects and neurodegenerative disorders.

The distribution and nature of age-related ubiquitin-positive granular structures (UPG) were examined in non-demented brains. In addition, their appearance pattern in some neurodegenerative disorders was investigated. In the transentorhinal cortex, they were distributed among cell islands of layer pre-alpha and in layers II and IIIab. In the amygdala, they were preferentially located in the accessory basal and basal nuclei. UPG were first observed in the transentorhinal cortex of non-demented middle-aged brains and increased in frequency and extended to other regions with increasing age. In Alzheimer-type dementia (ATD), they decreased with advance of the clinical stage. In diffuse Lewy body disease (DLBD), they decreased, accompanying linear neuritic structures. With the double-immuno-staining, UPG were frequently overlapped with neurofilament-positive granules. The multipolar cells of layer pre-alpha and pyramidal cells of layers IIIc and V were also immunostained with anti-neurofilament antibody, and the obliquely ascending fibers of these cells were found frequently to continue to these neurofilament-positive granules. Using ubiquitin immunoelectron microscopy, UPG appeared to derive from degenerating terminal axons. These findings suggest that UPG originate mainly from the recurrent collateral ascending axons in layers II-IIIab and from projecting axons in the amygdala. The occurrence of UPG in the limbic system is an important morphological hallmark of aging. In addition, further studies on the appearance pattern of UPG in ATD and DLBD may clarify whether a difference in the degenerative process of both disorders exists.

Adolescent↗
PubMed1996

Possible role of splice acceptor site in expression of unspliced gag-containing message of Moloney murine leukemia virus.

Moloney murine leukemia virus (MLV) having the gag coding region alone, G3.6, produced a low level of mRNA (1/10 of the wild-type level). Ligation of 441 nucleotides (nt) containing a splice acceptor (SA) site to the downstream portion of the remaining gag region restored the level of the unspliced message, simultaneously activating a cryptic splice donor (SD) site in the middle of the p30 coding region (between nt 1596 and 1597). Ligation of the 441 nt in the same site in the inverted orientation also increased the level of the unspliced message, activating the same SD site (between nt 1596 and 1597) and a new SA site just in front of the inserted 441 nt (between nt 4770 and 4771). Deletion or inversion of the 441-nt SA sequence from the wild-type MLV or from int in-frame deletion or int frameshift mutant MLVs of nearly full size resulted in the loss of spliced mRNA and concomitantly in a severe reduction of the unspliced mRNA, particularly at 37 degrees C. Deletion of the 5' SD site did not result in the reduction of the unspliced-mRNA level. When the gag region in G3.6 was replaced with a Neo(r) coding region, the level of expression was high. The data taken together suggest that the presence of an SA signal is necessary for high-level expression of unspliced mRNA encoding Gag or Gag-Pol.

3T3 Cells↗
PubMed1995

Investigation of tau-2 positive microglia-like cells in the subcortical nuclei of human neurodegenerative disorders.

An anti-tau monoclonal antibody tau-2 was demonstrated to react with the cells which characteristically appeared in the subcortical nuclei of certain neurodegenerative disorders. These cells had rod-like cell bodies and elongated processes, whose morphology was consistent with that of reactive microglia (tau-2 positive microglia-like cells; TPMC). TPMC were diffusely scattered in the subcortical nuclei, especially the putamen, irrelevant to focal tissue injury such as infarcts and amyloid deposits. TPMC were positively immunostained with anti-ferritin antibody, but negatively with LN3, anti-GFAP, other kinds of anti-tau and anti-neurofilament antibodies. TPMC were found in some cases of Alzheimer type dementia and diffuse Lewy body disease, but not in the cases of Parkinson's disease, Pick's disease and control without neurological disorder. Similar microglia-like cells were found around infarctic foci and amyloid cores of senile plaques, regardless of the disorder. They were, however, different from TPMC in that they were positively immunostained with LN3.

Aged↗
PubMed1995

Targeted infection of a retrovirus bearing a CD4-Env chimera into human cells expressing human immunodeficiency virus type 1.

We constructed a hybrid Moloney murine leukaemia virus (MoMLV) bearing both a chimeric CD4 and the wild-type MoMLV envelope protein (Env) on its surface. The chimeric molecule, consisting of a surface domain of CD4 and the C-terminal two-thirds of MLV Env, was expressed on the cell surface. When expressed in MoMLV-infected cells, the CD4-Env chimera was incorporated into the virion as efficiently as the wild-type MoMLV Env. The hybrid MoMLV could infect human HeLa cells (although not with high efficiency) only if the cells were expressing human immunodeficiency virus type 1 genome. This method of ligand incorporation into a virion may lead to a development of a cell-specific retroviral vector for targeting gene therapy.

3T3 Cells↗
PubMed1994

Interaction between the dominant negative mutant and the wild-type envelope proteins of Friend murine leukemia virus.

Interaction between the previously obtained dominant negative mutant, referred to as fcr (T. Matano, T. Odawara, M. Ohshima, H. Yoshikura, and A. Iwamoto, J. Virol. 67:2026-2033, 1993), and the wild-type envelope proteins (Env) of Friend murine leukemia virus was examined. The wild-type Env was bound to the fcr mutant Env and trapped in the endoplasmic reticulum. The virus receptor was not involved in this interaction.

Cell Line↗
PubMed1993

trans-dominant interference with virus infection at two different stages by a mutant envelope protein of Friend murine leukemia virus.

A dominant negative mutant Friend murine leukemia virus (FMLV) env gene was cloned from an immunoselected Friend erythroleukemia cell. The mutant env had a point mutation which resulted in a Cys-to-Arg substitution at the 361st amino acid in the FMLV envelope protein (Env). The mutant Env was retained in the endoplasmic reticulum (ER) and accumulated because of its slow degradation. The NIH 3T3 cells expressing the mutant env were resistant to ecotropic Moloney MLV (MoMLV) penetration, suggesting that the mutant Env traps the ecotropic MLV receptors in the ER. When the mutant env gene was transfected into and expressed in the cells persistently infected with MoMLV, the wild-type Env was trapped in the ER, and the MoMLV production was suppressed. Thus, the mutant Env accumulating in the ER trans-dominantly and efficiently interfered with the ecotropic MLV infection at both the early and the late stages.

3T3 Cells↗
PubMed1991

Epigenetic control of tumor cell morphology.

XC cell line derived from a single rat cell transformed by the Prague strain of Rous sarcoma virus produced morphologically different colonies. Among them, two distinct cell types consisting of thick, fusiform cells (L-type), and of flat, polygonal cells (R-type) were apparent. By repeated subclonings, pure cultures, L1 and R1, respectively, were obtained. These clones underwent morphological conversion during prolonged culture; L-type colonies appeared in the R-type clone and vice versa. The kinetic curve suggested that the conversion was multi-stepped. When inoculated into nude mice, L-type cells produced much larger tumors at a higher frequency than R-type cells, and the tumors induced by these two clones were histologically different. The expression of v-src gene was higher in L-type than in R-type cells at both mRNA and protein levels.

Actins↗
PubMed1991

Analysis of Moloney murine leukemia virus revertants mutated at the gag-pol junction.

Among Moloney murine leukemia viruses (Mo-MuLVs) having stop codons other than UAG at the gag-pol junction, Mo-MuLV with UAA, but not with UGA, had a replication disadvantage. Mo-MuLV with a glutamine codon (CAG) at the junction did not replicate. A revertant of this virus consisted of the original virus and a virus with a deletion of the pol region. Protease and Pr65gag encoded by their respective genomes complemented each other.

3T3 Cells↗
PubMed1986

Antitumor effect of adriamycin entrapped in liposomes conjugated with monoclonal antibody against tumor-associated antigen of bovine leukemia cells.

Monoclonal antibody against tumor-associated antigen (TAA) expressed on bovine leukemia cells was conjugated to liposomes containing adriamycin (ADM), and the specificity and therapeutic effects of the conjugates were examined in vitro and in vivo using a TAA-positive bovine leukemia cell line as the target tumor. In vitro studies with the TAA-positive cell line clearly indicated that the antibody-conjugated liposomes containing ADM exerted selective effects on TAA-positive cells in the inhibition assay of 3H-thymidine incorporation. Three injections of liposomes containing ADM (4 mg/kg) into tumor-bearing nude mice significantly inhibited the tumor growth and the therapeutic effect of the antibody-conjugated liposomes was far greater than that of normal mouse IgG-conjugated liposomes as assessed in terms of tumor size.

Animals↗
PubMedDate not supplied

An autopsied case of juvenile parkinsonism and dementia, with a widespread occurrence of Lewy bodies and spheroids.

An autopsied case of juvenile parkinsonism and dementia is described. The patient is a 48-year-old man who had a ten-year history of parkinsonian syndrome and progressive dementia. Neuropathological examination revealed a widespread occurrence of Lewy bodies and spheroids in the central nervous system. Lewy bodies were found not only in the brain stem and diencephalon, but also in the cerebral cortex. Massive numbers of small spheroids were observed in the globus pallidus, substantia nigra, mamillary bodies and hippocampus. Electron microscopical examination showed that most spheroids were composed of degenerative organelles with only a few neurofilaments, and were different from those of Hallervorden-Spatz disease. There was also marked neuronal loss with gliosis in the CA3-4 of the hippocampus. Some neurofibrillary tangles occurred in the hippocampus, subcortical and brain stem nuclei, but senile plaques were absent. This case may represent an atypical form of pure diffuse Lewy body disease.

Brain↗