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T Katagiri

Publications and source records attributed to T Katagiri.

At least 271 records · Page 15Linked to original sources
PubMed1990

Transforming growth factor-beta modulates proliferation and differentiation of mouse clonal osteoblastic MC3T3-E1 cells depending on their maturation stages.

The effect of transforming growth factor-beta (TGF-beta) on proliferation and differentiation of mouse clonal osteoblastic cells (MC3T3-E1) was examined in vitro in three different stages of their differentiation. Stage I (1-3 days after plating) was characterized by rapid cell growth, negligible alkaline phosphatase (ALP) activity and high proteoglycan synthesis, but low collagen production. In stage II (3-5 days after plating), proteoglycan synthesis sharply decreased and ALP activity and collagen synthesis began to increase. Stage III (7-9 days after plating) was characterized by maximal osteoblastic phenotypes. Treating MC3T3-E1 cells with 1 ng/ml of TGF-beta greatly inhibited DNA synthesis in stage I but not in stage II. In contrast, TGF-beta dose-dependently stimulated the synthesis of collagenase digestible proteins (CDP), noncollagenous proteins (NCP) and proteoglycan, especially in stage II. The minimum effective dose of TGF-beta in this stage was as low as 0.04-0.2 ng/ml. In stages I and III, the MC3T3-E1 cells were rather insensitive to TGF-beta in increasing three osteoblastic phenotypes. The increase in ALP activity in stages II and III was inhibited by 1 ng/ml of TGF-beta. These results indicate that the response to TGF-beta of mouse clonal osteoblastic MC3T3-E1 cells changes depending on their maturation stages.

Alkaline Phosphatase↗
PubMed1990

[Surface markers and function of T cells forming clusters with autologous dendritic cells].

Human peripheral dendritic cells form characteristic cell aggregates (clusters) with autologous T cells. We investigated the surface markers and function of the T cells that formed these clusters. The T cells that formed clusters were mainly CD4 positive, while CD8 positive cells were few. Moreover, the T cells that formed clusters were mostly 2H4 positive. However, some were 4B4 positive. These data showed that the T cells that formed clusters were mainly CD4 positive-2H4 positive cells. The function of the T cells that formed clusters was also investigated. These T cells significantly inhibited PWM-induced immunoglobulin production from autologous lymphocytes compared with non-clustered T cells. Or data indicated that the T cells that formed clusters were mainly suppressor-inducer T cells.

Antigens, Surface↗
PubMed1990

[A case of suspected allergic granulomatosis and angiitis with a rapid clinical course of paraplegia].

A 68-year-old man with suspected allergic granulomatosis and angiitis is reported. He had received 10 mg of prednisolone daily since July 1988 for asthma. He abruptly developed muscle weakness of the lower extremities, followed two days later by paraplegia. Six days after the onset of the muscle weakness, he was hospitalized. He showed disturbance of recent memory, disorientation, neck rigidity, paraplegia, mild muscle fasciculation and hypesthesia. He also showed paralytic ileus. Laboratory findings showed leukocytosis (24580/mm3), eosinophilia (56% of the peripheral white blood cells and 19% of the cells in the cerebrospinal fluid), on erythrocyte sedimentation rate of 31 mm/h, and the IgE level of 1200 IU/ml. The ECG showed loss of the r-wave in V1 and V2. A granulomatous lesion anterior to the spinal cord was found on myelography and MRI. Prednisolone was given at a dose of 60 mg daily resulting in improvement of the clinical symptoms and eosinophilia. There was disappearance of the granuloma on MRI performed after prednisolone therapy. Despite the severe manifestation of allergic granulomatosis and angiitis, prednisolone therapy had a marked effect in this patient. The granulomatous lesion anterior to the spinal cord shown by MRI suggested an eosinophilic granuloma, and may have been the etiology of some of the neurological symptoms.

Aged↗
PubMed1989

Capacities of a newly established thymic stromal cell clone to express Ia antigens and to produce interleukin-6, colony-stimulating factor, and thymic stroma-derived T-cell growth factor.

Thymic stromal cell lines, termed MRL104 and MRL28, have been isolated from long-term liquid cultures of thymic stromal cells from MRL/l mice. The capacities of these parental lines and derived clones to express Ia antigens and to produce cytokines involved in T-cell proliferation and/or differentiation were investigated. Parental lines and their clones did not exhibit a typical fibroblastic, macrophage-like, or epithelial appearance in electron as well as phase-contrast micrographs. These thymic stromal cells seemed to differ from established fibroblast lines in that these thymic stromal cells expressed Ia antigens after exposure to interferon-gamma (IFN-gamma), whereas fibroblast lines did not. They also appeared to differ from macrophage cell lines in that they lacked the expression of Mac-1 antigens on their cell surface and produced no detectable level of interleukin-1 (IL1) before or even after exposure to lipopolysaccharide. When these parental lines and its clones were tested for their ability to produce various types of cytokines, it was revealed that they were capable of producing colony-stimulating factor (CSF), IL6, and thymic stroma-derived T cell growth factor (TSTGF), which was recently described, but were unable to generate other lymphokines and IFNs. Thus these cell lines and clones represent unique features in that they have potentials to express Ia antigens and to produce CSF, IL6, and TSTGF. The biological significance for the expression of these features is discussed in the context of intrathymic T-cell maturation and T-cell repertoire selection.

Animals↗
PubMed1989

Lewy body-like hyaline inclusions in sporadic motor neuron disease are ubiquitinated.

Round eosinophilic hyaline inclusion bodies with halos in the somata of anterior horn cells from a case of sporadic lower motor neuron disease (MND) were intensely immunostained with the monoclonal anti-ubiquitin antibody (DF2). A few similar, DF2-positive inclusions were also observed in the nerve cell processes of anterior horn cell or in the neuropil. Most inclusions showed intense homogeneous staining of the entire inclusion, whereas a few had intense staining of their periphery with no or pale staining of the central areas. Other DF2-positive structures in the somata of anterior horn cells included cytoplasmic granular structures, eosinophilic thread-like or reticular structures, and small eosinophilic profiles different from Bunina bodies. The DF2-staining intensity of Bunina bodies and spheroids did not exceed the background level. These results suggest that ubiquitination is associated with a pathological process of anterior horn cell degeneration in this MND case.

Aged↗
PubMed1989

Overexpression of src family gene for tyrosine-kinase p59fyn in CD4-CD8- T cells of mice with a lymphoproliferative disorder.

Overexpression of a src family gene, lck, has been associated with differentiation of the murine thymic lymphoma line LSTRA. Recent findings by several groups strongly suggest a functional role for the gene product p56lck protein-tyrosine kinase (PTK) in the activation of normal T cells. A single recessive gene, lpr or gld, induces a lymphoproliferative disorder concomitant with autoimmune disease in mice. In this study, a 10-fold elevated activity of PTK encoded by fyn, another src family gene, was demonstrated in CD4-CD8- T cells in mutant mice. The increased PTK activity was consistent with overexpression of fyn mRNA. The elevated fyn mRNA expression appeared to be a characteristic of CD4-CD8- T cells, since it was not observed in normal T cells at any stage of differentiation. The fact that fyn mRNA expression was markedly induced in normal T cells by mitogenic stimulation with anti-T3 epsilon antiserum supports the possibility that p59fyn PTK is a signal-generating molecule in T cells. Thus, our findings provide insight into the physiological role for a src gene family kinase in T-cell development and contribute to a better understanding of the molecular mechanisms of disease-inducing recessive genes.

Animals↗
PubMed1989

Tyrosine phosphorylation of a c-Src-like protein is increased in membranes of CD4- CD8- T lymphocytes from lpr/lpr mice.

Mice homozygous for the autosomal recessive lpr gene have a disorder that results in autoimmunity and massive accumulation of T lymphocytes lacking CD4 and CD8 surface markers. These abnormal T cells exhibit constitutive tyrosine phosphorylation of a component of the CD3-T-cell receptor complex. We compared membrane tyrosine phosphorylation in lpr/lpr CD4- CD8- T cells and control T cells, lpr membranes exhibited a 7.3-fold increase (n = 16) in tyrosine phosphorylation of a 60-kilodalton protein. The increase was correlated with the Lpr but not the CD4- CD8- phenotype in that p60 phosphorylation was not increased in membranes from normal CD4- CD8- thymocytes. To identify the p60 in lpr cells, we examined the activity of several T-cell tyrosine-specific protein kinases. p56lck phosphorylation was only slightly increased in lpr membranes (2.2-fold; n = 16). Phorbol ester treatment of intact T cells before membrane isolation caused p56lck to migrate as pp60lck; however, pp60lck could be clearly distinguished from the pp60 in lpr cells by two-dimensional gel electrophoresis. The pp60 from lpr cells exhibited several isoforms at pH approximately 6.3 to 6.5. Although on two-dimensional gels pp60c-src had a pI (6.4 to 6.8) within a similar region, p60c-src mRNA, protein, and kinase activities were not increased in lpr cells. In addition, staphylococcal V8 proteolytic cleavage of the lpr pp60 isolated on two-dimensional gels yielded two major fragments, a pattern distinct from that of pp60c-src. However, by using an antiserum against the C-terminal sequence of c-Src and other related kinases, including p59fyn, the pp60 could be immunoprecipitated in greater amounts from lpr than from control T cells. When pp59(fyn) was selectively immunoprecipitated from T-cell membranes with specific antisera, its molecular weight, proteolytic cleavage pattern, and behavior on two-dimensional gels were identical to those of the pp60 from lpr cells. We conclude that p59(fyn) phosphorylation is increased in membranes from lpr/lpr CD4(-) CD8(-) T cells and that the increase is correlated with constitutive tyrosine phosphorylation and perhaps with the expansion of this unusual T-cell population.

Animals↗
PubMed1989

Protection of acute ischemic myocardial injury by pharmacological intervention.

Pharmacological protection of acute ischemic myocardial injury was studied using diltiazem, bunazosin, coenzyme-Q10 (Co-Q), and nicorandil, in dogs of which the left anterior descending coronary artery was ligated for 60 min. Drugs were given intravenously prior to and/or during coronary ligation. Co-Q, bunazosin and diltiazem suppressed degradation of sarcoplasmic reticulum (SR) expressed as inhibitions of reduction in Ca++-dependent ATPase activity and degradation of major ATPase protein. Fine structures of ischemic myocardial cells were simultaneously retained as well. On the contrary, the effects of nicorandil on ischemic myocardial injury were few. It is likely that protection of ischemic myocardial injury could be expected with drugs which react with ischemic myocardium directly and inhibit excess inflow of extracellular Ca++ in ischemic myocardium.

Adenosine Triphosphatases↗
PubMed1989

Comparative study on computed tomography and neurotological findings in spinocerebellar degeneration.

The classification of SCD on the basis of the neurotological findings was with classification based on CT findings in 40 cass of SCD. The areas of pons, cerebellar hemisphere, vermis and posterior fossa on CT films were measured by craniometer, and were compared in order to estimate the degree of atrophy. From these assessments, patients were classified into 3 types as follows; (1) 14 cases of cerebellar type, (2) 9 cases of brain stem type and (3) 17 cases of combined type. The classification of SCD based on the neurotological findings including the findings of gaze test, positioning test, eye tracking test, OKN, and fixation suppression test of caloric nystagmus, was well correlated to the classification based on CT findings. From the results, neurotological examination was demonstrated to make a contribution to the estimation of lesions and types in SCD.

Caloric Tests↗
PubMed1989

[Prediction of future physical work capacity based on serial echocardiography in patients with acute myocardial infarction].

The future physical work capacity of patients with myocardial infarction was predicted based on echocardiograms recorded during the acute stage. Subjects consisted of 55 patients with initial myocardial infarction who were admitted to the CCU within 24 hours after their attacks (anterior 26, inferior 23, non-transmural 6; age 24-85 years). Subjects were categorized in the good tolerance group (greater than or equal to 5.0 Mets; 35 cases) and poor tolerance group (less than 5.0 Mets, or incapable of performing the test; 20 cases) based on multi-stage exercise tests before discharge. These two groups were compared as to their serial echocardiograms made during the two weeks after onset, their maximum myocardial enzyme values, and hemodynamics (catheterization and coronary angiography) on admission and in the chronic stage. Left ventricular dimension did not change in the good tolerance group, but increased in the poor tolerance group. Left atrial dimension showed the same tendency. In the poor tolerance group, the amplitude of the mitral valve echo was smaller, and the A/R ratio of left ventricular inflow velocity was higher, compared with the good tolerance group, though maximum values of myocardial enzyme and coronary angiographic findings were similar. Pulmonary artery and capillary wedge pressures in the acute stage were higher, and cardiac index and left ventricular ejection fraction were lower in the poor tolerance group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Characterization and functional allotment of proto-oncogenes belonging to the src family.

Eight proto-oncogenes encode cytoplasmic protein tyrosine kinases whose primary structures are closely related to that of p60proto-src. This group of related genes is called the src-family. Their products share common structures: namely, a glycine residue at position 2 from the N terminus, a unique domain, a modulatory domain (SH2, SH3), a kinase (catalytic) domain, and a regulatory domain. Oncogenic activation of these genes may occur by various mutations such as 1) deletion or substitution of the tyrosine at the C-terminal position, 2) mutation at a defined position in the kinase domain or 3) deletion or mutation in the modulatory domain. The expressions of the proto-oncogenes of this family are tissue specific and are unique for each gene, suggesting functional allotment of these gene products. In the hematopoietic system, the genes appear to be expressed in specific cell lineages. In this paper, the functional allotments of these genes in the hematopoietic system are considered with special reference to the functions of lck, lyn, and fyn in cells of T and B lymphocyte lineages.

Amino Acid Sequence↗
PubMed1989

[Effect of lobenzarit disodium (CCA) on B cell differentiation to antibody secreting cells].

We investigated the effect of the immunomodulator CCA on B cells, using the system of Staphylococcus aureus Cowan 1-stimulated B cells developing into antibody secreting cells in the presence of T cell factors. Results were expressed as the number of plaque-forming cells (PFC), as measured by reverse hemolytic plaque assay. Serially diluted CCA was added to the culture system to evaluate its effect (500-0.005 micrograms/ml). Different results were obtained by adding CCA at a high dose or a low dose. High-dose CCA showed an inhibitory effect on PFC (p less than 0.01). On the other hand, low-dose CCA showed an inhibitory effect on high PFC responses of B cells and a stimulatory effect on low responses. Our data suggest that CCA has a direct effect on B cells and that low-dose CCA has immunomodulatory action on normal variations in immune responses.

Antibody-Producing Cells↗
PubMed1989

[A case of antigranulocyte antibody positive Felty's syndrome and its efficacy of plasmapheresis].

The patient is a 44-year-old female case of RA having a history of 10 years after onset, being admitted due to fever accompanied by granulocytopenia. By laboratory findings, WBC was 1,900/mm3, CRP 5+, RA 2+, RAHA 80 times, LE cells positive, antinuclear antibody strongly positive, granulocyte-specific antinuclear antibodies positive, and granulocyte specific cytotoxicity test strongly positive. Examination of bone marrow smears revealed, the cell numbers tended to decrease in the neutrophil maturity phase. The case was diagnosed as Felty's syndrome because of the obvious splenomegaly and leukopenia. Administration of 30 mg/day of prednisolone was not sufficient in effect, and plasmapheresis was conducted concomitantly. As a result, the granulocyte count increased and the granulocyte cytotoxicity titer was lowered. It is hence suggested that the antigranulocyte antibodies are responsible for the mechanism of granulocytopenia in this case, and the possibility of promotion of destruction in the periphery was inferred, and it is accordingly considered useful to combine administration of small dose of adrenocortical steroid preparation with plasmapheresis for the treatment of this disease.

Adult↗
PubMed1988

A comparison of the distributions of eight peptides in spinal cord from normal controls and cases of motor neurone disease with special reference to Onuf's nucleus.

The distributions of 8 peptides were studied in the 4 major segmental levels (cervical, thoracic, lumbar, sacral) of the spinal cord in 52 neurologically normal cases. Similar regions from 36 cases of motor neurone disease (MND) were compared using the same procedures to determine possible changes in the distribution of peptides in areas associated with sensory, motor and autonomic function. In normal spinal cords, calcitonin gene-related peptide (CGRP)-, the C-flanking peptide of neuropeptide Y (CPON)-, enkephalin-, galanin-, neurokinin-like-, somatostatin- and vasoactive intestinal polypeptide (VIP)-immunoreactive fibres were abundant in the dorsal horn. Numerous somatostatin-immunoreactive cell bodies were also present. In the ventral horn, immunoreactive fibres were less abundant. Most motoneurones were closely apposed by fibres immunoreactive for enkephalin, neurokinin, somatostatin and thyrotrophin-releasing hormone (TRH). A subpopulation of motoneurones, most notable in lumbar segments, displayed CGRP immunoreactivity. In common with autonomic nuclei, Onuf's nucleus, which is thought to innervate perineal striated muscle and external urethral and anal sphincters, was densely innervated with CPON-, enkephalin-, and in particular somatostatin-immunoreactive fibres, thus suggesting Onuf's nucleus may have an autonomic component. In the diseased cords, there was a reduction in the area of the ventral horn and numbers of motoneurones as revealed by conventional histological staining and immunostaining of neurofilament triplet proteins. No changes in the distribution of peptides was noted in the dorsal horn or autonomic nuclei. By contrast, in the ventral horn, neurokinin-, enkephalin-, somatostatin- and TRH-immunoreactive fibres, which are normally found associated with motoneurones, were absent. Therefore, not only are motoneurones lost in MND, but also the fibres which innervate them. CGRP-immunoreactive motoneurones were not observed, a finding consistent with the proposed role of this peptide as a muscle-trophic factor. In contrast to the large motoneurone groups in the ventral horn, the neuronal integrity of Onuf's nucleus and the peptides associated with it were spared. These data further imply that Onuf's nucleus is not a typical motor nucleus and it is not purely somatic. The coincident loss of peptide immunoreactivity and motoneurones from the large motor nuclei and sparing of Onuf's nucleus and its peptide-containing constituents in the diseased state suggests that peptides contribute to maintenance of neural integrity.

Adolescent↗
PubMed1988

Two different molecular pathways account for low IL-2 receptor and c-myc mRNA expression by lpr Lyt-2- L3T4- T cells.

We have previously shown that Lyt-2- L3T4- T cells from the lymph nodes of MRL/lpr/lpr mice could respond to 12-O-tetradecanoylphorbol-2-acetate (TPA) and A23187 by proliferation, IL-2 secretion, and IL-2R (IL-2R) expression. However, the optimal response was significantly less than that of normal T cells. To understand the molecular mechanisms underlying the relatively inert nature of these cells, the expression of the T cell early competence genes, IL-2R and c-myc, was examined by Northern blot analysis and nuclear run-on assays. In resting lpr Lyt-2- L3T4- T cells, IL-2R mRNA was not detected, whereas the expression of c-myc mRNA was slightly enhanced compared to that of normal T cells. TPA and A23187 synergistically induced both IL-2R and c-myc mRNA expression by the lpr Lyt-2- L3T4- T cells, as well as by normal T cells. However, the amounts of specific mRNA induced in the former were much less than those in the latter. Cycloheximide treatment caused the TPA/A23187-stimulated lpr cells to express large amounts of c-myc mRNA, but not IL-2R mRNA. The deficient expression of c-myc and its correction by cycloheximide treatment were also observed in Con A-stimulated lpr Lyt-2- L3T4- T cells. Run-on transcription assays revealed that the enhancing effect of cycloheximide was most likely at the posttranscriptional level. These findings suggest that two separate mechanisms differentiated by their sensitivity to cycloheximide can inhibit the accumulation of mRNA for early competence genes in lpr Lyt-2- L3T4- T cells. These mechanisms may prevent the full activation of the lpr T cells and lead to abnormal differentiation of these cells.

Animals↗
PubMed1988

The lpr gene causes an intrinsic T cell abnormality that is required for hyperproliferation.

The lpr gene induces marked lymphoproliferation characterized by the massive accumulation of T cells of an unusual phenotype and concomitant autoimmune disease. To clarify the mechanism of the lpr effect, bone marrow cells from B6-lpr/lpr (Ly-1.2) and B6-+/+ (Ly-1.1) mice were transferred into lethally irradiated B6-lpr/lpr mice. As has been previously reported, recipients of the B6-lpr/lpr bone marrow showed the typical lpr phenotype with marked lymphadenopathy, splenomegaly and increased levels of autoantibodies; while the recipients of B6-+/+ bone marrow had normal sized lymph nodes and spleen and no autoantibodies. A third group of mice received an equal mixture of bone marrow cells from the B6-lpr/lpr and B6-+/+ donors. These mice showed both lymphadenopathy and autoantibody production comparable to that of recipients of the B6-lpr/lpr marrow alone. Immunofluorocytometric analysis of the lymphoid populations in these mixed bone marrow recipients established that the T cells from the lpr/lpr and +/+ donors were equivalently represented in the peripheral blood and thymus. In striking contrast, the T cells that accumulated in abnormally large numbers in the lymph nodes were almost entirely from the lpr donor. Their surface phenotype was Thy-1+(dull), Ly-1.2+(dull), Lyt-2-, L3T4-, 9F3+, and 3A1+, which is consistent with that found in intact lpr mice. These results indicate that the lpr gene causes an intrinsic defect directly within the T cells that accumulate in large numbers in lpr mice. In addition, the presence of the +/+ T cells cannot prevent the expression of the lpr abnormalities.

Animals↗