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Biomedical subjects

J Murata

Publications and source records attributed to J Murata.

At least 91 records · Page 5Linked to original sources
PubMed1993

Human glioblastoma cells produce granulocyte-macrophage colony-stimulating factor in vitro, but not in vivo, without expressing its receptor.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) production and receptor expression by human glioblastomas was studied. Enzyme-linked immunosorbent assay showed four of 10 glioblastoma cell lines spontaneously released GM-CSF (2.9-9.2 pg GM-CSF protein/ml culture medium), which was enhanced by stimulation with tumor necrosis factor-alpha (TNF) (10 U/ml) up to 410 pg/ml. TNF also induced secretion of GM-CSF by another cell line. Northern blot analysis identified increasing GM-CSF gene expression by cells following TNF stimulation. However, no GM-CSF protein was detectable in the cerebrospinal fluid of three malignant glioma patients. Intratumoral administration of TNF in the patients also failed to stimulate GM-CSF levels in the cerebrospinal fluid. A binding assay using flow cytometry with biotinylated GM-CSF and Scatchard analysis using 125I-labeled GM-CSF failed to demonstrate GM-CSF receptor expression on the 13 cell lines. Exogenous GM-CSF stimulation had no effect on production of prostaglandin E2, interleukin-6, or interleukin-8 by glioma cells. Human glioblastoma cells secrete GM-CSF without expressing the receptor in vitro, but there was no evidence of GM-CSF production in vivo.

Glioblastoma↗
PubMed1993

Morphological aspects of transport of potassium ion in the marginal cell.

Structure and function of the marginal cell in the stria vascularis were studied by freeze-fracture, cytochemistry and immunohistochemistry with special regard to the ion transport of potassium. Freeze-fracture showed that marginal cells were connected by tight junctions beneath the scala media K(+)-NPPase cytochemistry showed that Na+, K(+)-ATPase was abundant on the basolateral infoldings of the marginal cell. Immunohistochemistry of a rat Isk protein, which has a property of a potassium channel, revealed that the rat Isk protein was localized at the endolymphatic surface of the marginal cell. These findings supported the 'one-pump' theory (Offner et al. Hear Res 1987; 29: 117-24).

Animals↗
PubMed1993

[A case of complete remission of breast cancer with bilateral multiple lung metastases by combination therapy of MPA, THP, CPM and 5-FU].

A 55-year-old female was admitted for right breast tumor with multiple bilateral lung metastases. Modified radical mastectomy (Auchincloss method) was carried out. And the combination chemoendocrine therapy was undertaken using CPA 100 mg p.o. days 1-18, THP 40 mg i.v. days 1, 8, 5-FU 500 mg i.v. days 1, 8 and MPA 1,200 mg p.o. daily. One month later, the lung metastases completely disappeared on chest CT gram. Nine courses of chemotherapy with the same drugs were undertaken intravenously every four weeks. This therapy has been continuously effective for one and half years now. These results suggested the importance of a severe adjuvant therapy for the initial phase of advanced breast cancer.

Administration, Oral↗
PubMed1992

Inhibition of tumor-induced angiogenesis by the administration of recombinant interferon-gamma followed by a synthetic lipid-A subunit analogue (GLA-60).

The effect of the administration of recombinant interferon-gamma (rIFN-gamma) and a synthetic lipid A subunit analog (GLA-60) on angiogenesis induced by B16-BL6 melanoma was examined in syngeneic C57BL/6 mice. Intravenous administration of rIFN-gamma followed by GLA-60 (referred to as rIFN-gamma/GLA-60) induced endogenous production of tumor necrosis factor (TNF). This treatment on day 3 after tumor inoculation caused a marked decrease in the number of vessels oriented towards the tumor mass (angiogenic response) and tumor size over a period of 9 days. In contrast, neither rIFN-gamma nor GLA-60 alone, nor GLA-60/rIFN-gamma (reverse sequence of administration), which is unable to induce the production of TNF in the serum, had any effect. Sera induced by the treatment with rIFN-gamma/GLA-60, and recombinant TNF, inhibited the in vitro growth of lung endothelial cells which is considered to be one of the essential events in tumor neovascularization. Multiple i.v. treatments with rIFN-gamma/GLA-60 on days 5, 8 and 11 after s.c. implantation of tumor significantly inhibited primary tumor growth by the amputation time (day 20) and lung metastasis of B16-BL6 cells on day 34, while other treatment modalities had no such effect. Our results indicate that inhibition of lung-tumor metastasis by rIFN-gamma/GLA-60 treatment may be partly due to the inhibition of tumor-associated angiogenesis.

Animals↗
PubMed1992

Differences in chemotaxis to fibronectin in weakly and highly metastatic tumor cells.

We have examined the chemotactic ability of tumor cell lines with different metastatic potential to plasma fibronectin in Transwell chamber assay. Human renal carcinoma cells with highly metastatic potential, SN12 C-2, chemotactically migrated to fibronectin (10 micrograms/ml) about three-fold more strongly than weakly metastatic SN12 C-4 cells. Similarly, murine melanoma B16-BL6 cells (highly metastatic) showed higher motility to soluble fibronectin in comparison with weakly metastatic B16-F1 cells. Anti-VLA-alpha 3 and beta 1 antibodies potently blocked the chemotaxis of both highly and weakly metastatic cells (SN12 C-2 and C-4) to fibronectin. This implies that the migration of both C-2 and C-4 cells to fibronectin is basically mediated by VLA-3 receptor. In contrast, the anti-VLA-alpha 5 antibody and RGDS peptide significantly inhibited the chemotaxis of SN12 C-2 cells to fibronectin, but did not affect weakly metastatic SN12 C-4 cells. These results suggest that the chemotactic ability to fibronectin positively correlates with the metastatic potential in SN12 and B16 cell lines, and that VLA-5 receptor is concerned in the motility of highly metastatic SN12 C-2 cells to soluble fibronectin.

Antibodies, Monoclonal↗
PubMed1991

Recombinant human granulocyte colony-stimulating factor inhibits the metastasis of hematogenous and non-hematogenous tumors in mice.

We studied the effects of in vivo administrations of recombinant human granulocyte colony-stimulating factor (rhG-CSF) on the metastasis of murine hematogenous and non-hematogenous tumors in spontaneous and experimental metastasis models. Spontaneous lung metastasis caused by intra-footpad injections of B16-BL6 melanoma and Lewis-lung-carcinoma (3LL) cells were inhibited by intravenous (i.v.) and subcutaneous (s.c.) injections of rhG-CSF after excision of the primary tumors. Recombinant hG-CSF significantly inhibited liver metastasis when administered i.v. after i.v. injection of L5178Y-ML25 T-lymphoma cells. Multiple i.v. administration of rhG-CSF after the tumor inoculation prolonged the survival times of mice inoculated i.v. with L5178Y-ML25 lymphoma cells. Recombinant hG-CSF did not directly affect the growth of B16-BL6 and L5178Y-ML25 cells in vitro. During the administration periods, both i.v. and s.c. injections of rhG-CSF increased the number of total white blood cells (WBC) in peripheral blood to approximately 3 times the normal level in normal and tumor-bearing mice. We also found that the administration of rhG-CSF stimulates neutrophils to become cytostatic against these tumor cells. Our results indicate that the injection of rhG-CSF is effective in inhibiting lung and liver metastases by activating neutrophils and increasing cell number.

Animals↗
PubMed1991

Inhibition of tumor-induced angiogenesis by sulfated chitin derivatives.

The effect of antimetastatic sulfated chitin derivatives (SCM-chitin III) on angiogenesis induced by B16-BL6 cells was examined in syngeneic mice. SCM-chitin III caused a marked decrease of the number of vessels toward tumor mass (angiogenic response) without affecting the tumor cell growth when coinjected with tumor cells (on day 0), or injected into tumor site on day 1 or 3 after tumor inoculation. In contrast, carboxymethyl chitin as well as heparin had no effect. Invasion of endothelial cells through reconstituted basement membrane (Matrigel) toward tumor-conditioned media was significantly inhibited by SCM-chitin III in a Transwell chamber assay. SCM-chitin III also inhibited the haptotactic migration of endothelial cells to fibronectin-substrate, but did not inhibit the chemotactic activity in tumor conditioned media in vitro. SCM-chitin III did not directly affect the viability and the growth of tumor cells and endothelial cells in vitro. These results suggest that inhibition of lung tumor metastasis by SCM-chitin III may in part be due to the inhibition of tumor-associated angiogenesis.

Animals↗
PubMed1991

Inhibitory effect of fibronectin and its recombinant polypeptides on the adhesion of metastatic melanoma cells to laminin.

We have utilized recombinant fibronectin fragments with cell-binding domain (C-274), heparin-binding domain (H-271) or CS1 peptide in type III connecting segment (IIICS) and their fusion polypeptides such as CH-296 (containing C-274, H-271 and CS1), CH-271 (containing C-274 and H-271) and C-CS1 (containing C-274 and CS1) to investigate the mechanism of the fibronectin-mediated inhibitory effect on tumor cell adhesion to laminin as well as fibronectin. These fragments retained cell adhesion-promoting and/or heparin-binding properties when they were immobilized on a surface. Pretreatment of tumor cells with CH-296 or CH-271 suppressed cell adhesion to both laminin and fibronectin. H-271 at the high concentration of 500 micrograms/ml slightly inhibited cell adhesion to laminin (but not to fibronectin), whereas C-274, C-CS1 or a mixture of C-274, H-271 and CS1 (similar molar ratio to CH-296) inhibited cell adhesion to fibronectin but not to laminin. On the other hand, tumor cell adhesion to laminin-substrate was also inhibited by heparin or heparan sulfate, which were able to bind to laminin, suggesting that heparin-like molecules on the cell surface may be included among the laminin receptors. These results indicated that the co-presence of cell- and heparin-binding domains of fibronectin may be required for the fibronectin-mediated inhibitory effect on tumor cell adhesion to laminin, and that the interaction of the heparin-binding domain of fibronectin with the cell surface leads to the inhibition of the cell adhesion to laminin.

Amino Acid Sequence↗
PubMed1991

Recombinant fusion polypeptide with cell- and heparin-binding domains of fibronectin inhibits liver metastasis of L5178Y-ML25 lymphoma cells.

We have investigated the effect of recombinant polypeptides with cell-binding domain (C-274) or with heparin-binding domain (H-271) and their fusion polypeptide (CH-271) on liver metastasis of murine lymphoid tumor. The polypeptides containing heparin-binding domain, H-271 and CH-271, were able to inhibit liver metastasis when co-injected i.v. with L5178Y-ML25 T-lymphoma cells, while C-274 with cell-binding domain showed much weaker antimetastatic activity. Treatment with H-271 or CH-271 substantially prolonged the survival time of mice injected i.v. with L5178Y-ML25 cells. CH-271, containing cell- and heparin-binding domains, was more antimetastatic than H-271. The reason why CH-271 was more effective in inhibiting liver metastasis than H-271 can not be explained in terms of a difference in the stability in the circulation or in the molecular size of the polypeptide. The polypeptides used in this study did not affect the tumor cell growth or viability in vitro. CH-271 was found to be still active in inhibiting liver metastasis even when natural killer cells or macrophages were removed from this system. Furthermore, multiple administrations of CH-271 after tumor implantation effectively inhibited liver metastasis and enhanced the survival rate as compared with H-271, C-274 and untreated control. Thus, the fusion of H-271 with C-274 (i.e. CH-271) augments the antimetastatic property of H-271, possibly through the interaction between tumor cells and the heparin-binding domain of fibronectin.

2-Chloroadenosine↗
PubMed1991

Inhibitory effect of antimetastatic fusion polypeptide of human fibronectin on tumor cell adhesion to extracellular matrices.

We investigated the inhibitory mechanism of liver metastasis by using recombinant fragments with cell- and/or heparin-binding domains (C-274, H-271 or the fusion fragment CH-271). Intravenous co-injection of L5178Y-ML25 cells with CH-271 was more effective for the inhibition of liver metastasis than C-274, H-271 or C-274 + H-271. Reduction of the arrest and retention of the radiolabeled tumor cells in the liver of mice was found when CH-271 was co-injected with tumor cells. L5178Y-ML25 cells adhered both concentration- and time-dependently to the substrates precoated with fibronectin, laminin and reconstituted basement membrane, Matrigel. The tumor cell adhesions to the substrates were inhibited in the presence of CH-271. The tumor cell interaction with CH-271-substrate was inhibited by heparin, and monoclonal antibodies (IST-1 or IST-2) against the heparin-binding domain of fibronectin. However, monoclonal antibodies against the cell-binding domain failed to block the interaction. Similarly, CH-271-mediated antimetastatic activity was also inhibited by the treatment of CH-271 with IST-1 before the co-injection with tumor cells, whereas monoclonal antibody against the cell-binding domain had no effect. Thus, the antimetastatic effect of CH-271 fusion fragment on liver metastasis of L5178Y-ML25 cells may be partly due to interference with the adhesive interaction of tumor cells with extracellular matrix or basement membrane components by a heparin-binding domain-dependent mechanism.

Animals↗
PubMed1991

Molecular properties of poly(RGD) and its binding capacities to metastatic melanoma cells.

We examined the binding capacity of anti-metastatic polypeptide containing repetitive Arg-Gly-Asp(RGD) sequence derived from cell binding site of fibronectin, poly(RGD), to the surface of tumor cells. Poly(RGD) competitively inhibited the binding of radiolabeled fibronectin to the cell surface more potently than oligo(RGD) or RGD tripeptide on a molar basis. Compared on a weight basis to oligo(RGD) or RGD peptide, poly(RGD) was more active than the oligo- and monomeric peptide at inhibiting tumor cell adhesion to immobilized fibronectin. The secondary structure of poly(RGD) was predicted to be a beta-turn from the data of CD spectra and its amino acid sequence. These findings suggest that poly(RGD)-mediated inhibition of cell adhesion is due to its potent binding capacity to fibronectin receptors on cell surface probably through its conformational properties.

Animals↗
PubMed1991

[A case report of hemangioma of the petrous bone which caused facial spasm and facial palsy].

A rare case of hemangioma of the petrous bone is described. A 31-year-old woman suffered from right facial twitching and palsy. So she underwent a craniectomy intending microvascular decompression of the facial nerve, but no compressing vessels or tumors were found. Three years later, however, her facial fasciculation disappeared spontaneously, but facial weakness deteriorated and she began to feel vertigo. On admission, neurological examination revealed right facial palsy of the peripheral type, slight hearing disturbance, and canal palsy. Bone-window CT and T2-weighted MRI revealed a small tumor destroying the petrous bone near the geniculate portion of the facial nerve. Using the epidural subtemporal approach, the tumor was totally removed and the facial nerve remained intact. Histologically it was diagnosed as hemangioma. Hemangioma of the skull base bone is rare, and it is interesting that the tumor in this case caused abnormal facial contraction like hemifacial spasm.

Adult↗
PubMed1991

[Intraoperative lumbar injection of Ringer's solution for surgical treatment of chronic subdural hematomas].

A series of 64 patients underwent surgical treatment for chronic subdural hematomas between 1980 and 1989. The procedure consisted of a single burr-hole, irrigation of the hematoma without subdural drainage and lumbar intrathecal injection of Ringer's solution. Irrigation was carried out until the washing was clear and the injection was continued until the brain was in contact with the edge of the burr-hole. Excellent outcome was achieved in 53 patients (82.8% of the total). Two of the patients died, thus making a 3.1% mortality rate. Such complications as tension pneumocephalus and intracerebral hematoma were not observed and no patient had a recurrence.

Adult↗
PubMed1990

Modulation of haptotactic migration of metastatic melanoma cells by the interaction between heparin and heparin-binding domain of fibronectin.

We utilized recombinant fibronectin polypeptides with cell-binding domain and heparin-binding domains (referred to as C-274 and H-271, respectively) and their fusion polypeptide (CH-271) to examine the role of sulfated polysaccharide heparin and/or the functional domains of fibronectin in modulating tumor cell behavior. Both C-274 and CH-271 polypeptides with cell-binding domains promoted the adhesion and migration of B16-BL6 melanoma cells, whereas H-271 did not. Heparin bound to the immobilized polypeptides with heparin-binding domain (H-271, CH-271, and a mixture of C-274 and H-271 or fibronectin) but did not affect the tumor cell adhesion to the substrates. At the same time, heparin or two monoclonal antibodies against the heparin-binding domain were able to inhibit the haptotactic migration to CH-271 or fibronectin, though not to C-274 or a mixture of C-274 and H-271. This suggests that although heparin did not affect tumor cell adhesion to the cell-binding domain near the heparin-binding domain in CH-271 or fibronectin, it did lead to a modulation of cell motility. It seems likely that the regulatory mechanism may depend on interaction between heparin-like molecules on the cell surface and the heparin-binding domain in fibronectin, rather than on simple steric hindrance or on the masking of the cell-binding domain caused by the binding of heparin to heparin-binding domain.

Animals↗
PubMed1990

Inhibition by sulfated chitin derivatives of invasion through extracellular matrix and enzymatic degradation by metastatic melanoma cells.

We have investigated the effects of sulfated chitin derivatives and heparin on the invasion of B16-BL6 melanoma cells through reconstituted basement membrane Matrigel which contains laminin, type IV collagen, heparin sulfate proteoglycan, and entactin. 6-O-sulfated chitin (S-chitin) and 6-O-sulfated and carboxymethyl chitin (SCM-chitin) significantly inhibited the penetration of tumor cells through Matrigel in parallel with the increased degree of sulfation. However, 6-O- and N-sulfated but partially N-deacetylated chitin derivative (SCM-chitosan) and CM-chitin had no effect. SCM-chitin with a high degree of sulfation (SCM-chitin III), which exhibited fairly low levels of anticoagulant activity, was more effective than intact heparin. SCM-chitin III and heparin were also shown to block the attachment and migration of tumor cells to laminin-coated substrates, which are considered to be involved in tumor invasion. The inhibition of cell attachment and migration by SCM-chitin III and heparin is likely to depend upon their specific binding to laminin molecules (possibly the heparin-binding domain). Degradation of heparan sulfate by heparanase was inhibited by SCM-chitin III and heparin in a dose-dependent manner. Surprisingly, SCM-chitin III could inhibit type IV collagenolytic activity of tumor cells more potently than heparin. Thus, nontoxic SCM-chitin III of low anticoagulant properties may provide a promising basis for the prevention of cancer metastasis.

Binding, Competitive↗
PubMed1990

Two flavonol glycosides from the underground parts of Vancouveria hexandra.

Two new flavonol glycosides were isolated from the roots and rhizomes of Vancouveria hexandra. The glycosides were determined by chemical and spectral means to be anhydroicaritin 3-galactosyl(1----3) rhamnoside-7-glucoside and anhydroicaritin 3-[6-O-acetyl-galactosyl(1----3)rhamnoside]-7-glucoside.

Flavonoids↗
PubMed1990

Production of interleukin 1 from human monocytes stimulated by synthetic lipid A subunit analogues.

We have investigated that synthetic lipid A subunit analogues (GLA compounds) as well as E. coli type lipopolysaccharide (LPS) and synthetic lipid A (compound 506) are able to stimulate human monocytes to release IL-1 in vitro. Of monosaccharide-type GLA compounds, GLA-60 was found to be more active for the induction of IL-1 production than GLA-59 and GLA-27, and similar to that of LPS or compound 506. GLA-60 could induce not only the secretion of IL-1 into culture supernatant but also the expression of membrane-associated form of IL-1 in human monocytes. Furthermore, no detectable IL-2 activity was observed in the culture supernatant. These results show that synthetic lipid A analogues of low toxicity, in particular GLA-60, are active in inducing IL-1 production in human monocytes.

Cell Division↗