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T Seya

Publications and source records attributed to T Seya.

At least 73 records · Page 4Linked to original sources

Cellular distribution of a GPI-anchored complement regulatory protein CD59: homodimerization on the surface of HeLa and CD59-transfected CHO cells.

Human glycosyl phosphatidylinositol-anchored protein CD59 was solubilized in detergent-insoluble complexes (DICs) and in post-nuclear pellets by a two-step solubilization procedure using Triton X-100 and octylglucoside. CD59 molecules are recovered in both fractions, the amount being greater in the latter fraction in all cell types tested. Specific labeling of surface CD59 molecules revealed that the CD59 detected in DICs originated from intracellular compartments, whereas that in post-nuclear pellets was in part derived from the cell surface. Cross-linking of surface proteins with chemical cross-linker followed by Western blotting with anti-CD59 antibody revealed cross-linked products with molecular masses of 28-36 kDa on HeLa and human CD59 cDNA-transfected CHO cells; the CD59-associating molecules were estimated to be 13-18 kDa in size. The cross-linked products were extracted in the post nuclear pellets, and CD59 existed mainly as a cross-linked form on the cell surface. Two-dimensional electrophoresis of the cross-linked products revealed no trace of molecules other than CD59. The cross-linked products showed the same N-terminal sequences as CD59 and a strikingly similar amino acid composition to that of CD59. Thus, most likely, the cross-linked products are CD59 dimers. The finding that CD59 localized on outer membranes is all in the form of dimers suggests the importance of dimerization for CD59 functioning.

Animals↗

Involvement of phosphoinositide 3-kinase in regulation of adhesive activity of highly metastatic hepatoma cells.

We have established hepatoma clones from benzopyrene-treated liver cells, one of which (G-5) shows extensive metastasis to the lung when injected subcutaneously into mice [Tanigaki, Y. et al. (1995) Invasion Metastasis 15, 70-80]. In the present study, we performed in vitro assays suitable for examination of the adhesive and invasive properties of the highly metastatic cells. G-5 cells efficiently entered the pores of fibronectin-coated filters. Treatment of the cells with an inhibitor of phosphoinositide 3-kinase (PI 3-kinase), wortmannin, significantly impaired the invasive activity. A structurally unrelated inhibitor, 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002) also prevented invasion. Both inhibitors suppressed cell adhesion to fibronectin-coated dishes. G-5 cells were next transfected with a mutant regulatory subunit (Deltap85) of PI 3-kinase, which was expected to impair the function of PI 3-kinase. The transfectants showed suppressed adhesion to the dishes and did not efficiently migrate into the filters. The lower adhesive ability of the transfected cells was not further affected by inhibitors of PI 3-kinase. Thus, PI 3-kinase activity contributes significantly to the adhesive and invasive properties of G-5 cells.

Androstadienes↗

Moesin is not a receptor for measles virus entry into mouse embryonic stem cells.

The involvement of moesin in measles virus (MV) entry was investigated with moesin-positive and -negative mouse embryonic stem (ES) cells. MV infection of these cells was very ineffective and was independent of moesin expression. Furthermore, when these cells were transfected to express human CD46, a 100-fold increase in syncytium formation was observed with these cells and was independent of the expression of moesin. The only obvious difference between moesin-positive and -negative ES cells was the shape of the syncytia formed. Moesin-negative ES cells expressing or not expressing human CD46 formed separate pieces of fragmented syncytia which were torn apart during spreading, whereas ES cells expressing moesin exhibited typical syncytia. In addition, moesin was not detected on the surface of any murine cells or cell lines that we have tested by a flow cytometric assay with moesin-specific antibodies. These findings indicate that murine moesin is neither a receptor nor a CD46 coreceptor for MV entry into mouse ES cells. Moesin is involved in actin filament-plasma membrane interactions as a cross-linker, and it affects only the spreading and shape of MV-mediated syncytia.

Animals↗

A wild-type Japanese measles virus strain inducing predominant early down-regulation of CD46.

Down-regulation of CD46 secondary to stimulation with measles virus (MV) was investigated using CD46-positive cell lines and Japanese wild-type MV strains. The cells used were simian cell lines B95a and Vero in which MV strains have been adapted to be amplified, and Chinese hamster ovary (CHO) cell transfectants expressing human CD46 with (CHO(tail+)) or without (CHO(tail-)) the cytoplasmic tail. Of four Vero-adapted and three B95a-adapted MV strains, one Vero-adapted strain named Khono (KO), down-regulated CD46 within 60 min (early down-regulation) in all cell lines examined except Vero. No strains other than Toyoshima (TY), which induced early down-regulation only in CHO(tail+) cells, induced early down-regulation of CD46 in any combination. On the other hand, conventional down-regulation of CD46 was observed 24 h post-MV inoculation (late down-regulation) when cell lines used were adapted to MV strains. Thus, we concluded that there are two modes of CD46 down-regulation by MV and the unique strain KO markedly induces early down-regulation. Also, the CD46 homologue of B95a, which fails to act as a MV receptor, is down-regulated concomitantly with MV replication (>24 h) in cells principally by competent virus strains.

Amino Acid Sequence↗

CD46 (membrane cofactor protein of complement, measles virus receptor): structural and functional divergence among species (review).

Human CD46 was identified as a complement regulator and was later shown to be a measles virus receptor. The ubiquitous distribution profile of CD46 accounted for systemic measles infection and general protection of host tissue/organs from autologous complement. A similar ubiquitous distribution was observed for swine and simian CD46 homologues based upon subsequent cDNA cloning and Northern analysis, reinforcing the roles of CD46. In contrast, recent cDNA cloning and distribution analyses of murine and guinea-pig CD46 revealed the predominant expression of these rodent CD46 homologues in the testis, especially in mature testicular germ cells. These results do not support the established functions of human CD46 but support the hypothesis that CD46 on sperm serves as a fertilization-related adhesion molecule toward eggs. Here, we review the structure, function and distribution of human CD46 and discuss the possible differences between human CD46 and its homologues recently cloned from a variety of non-human primates and other animals.

Amino Acid Sequence↗

The regulation of membrane cofactor protein (CD46) expression by the 3' untranslated region in transgenic mice.

Regulation of the membrane cofactor protein (MCP: CD46) was examined. While the expression of MCP in mice carrying MCP(BC2) cDNA with 125 bp of 3' untranslated region (3'UT) was minimal, that in mice carrying MCP cDNA without total 3' UT was evident in many organs. Reverse transcriptase polymerase chain reaction (RT-PCR) analysis clearly showed the presence of mRNA even in transgenic mice with 3' UT, suggesting that the expression was regulated at the post-transcriptional stage. The in vitro expression data of MCP molecules on the stable Chinese hamster ovary (CHO) cell clone corresponded to that in transgenic mice. The first 125 bp downregulated the expression of MCP molecules in combination with not only beta-actin, but also SR alpha, promoter. Also, this region inhibited expression of decay accelerating factor (DAF: CD55) molecules when it was inserted into cDNA of DAF. Furthermore, the first 32 bp of the 3' UT revealed the same downregulation effect as 125 bp on MCP molecules. These findings indicated that the first 125 bp (and the first 32 bp in particular) of 3' UT regulate the expression of MCP molecules in transgenic mice.

Animals↗

Molecular cloning and sequence analysis of the cDNA for the mouse counterpart to adult hamster liver purified growth inhibitory factor.

A cDNA clone encoding the mouse counterpart to adult hamster liver purified growth inhibitory factor (PGIF) was isolated from a mouse liver cDNA library by using antibodies raised against PGIF and sequenced. It contained a single open reading frame with a coding capacity for a 323 amino acid protein. Sequence analysis showed that it shared high homology with rat- and human liver arginases: the cDNA clone was 92% identical for rat arginase at the nucleotide level and was 93% identical to it at the deduced amino acid level. These results suggest that PGIF derived from adult hamster liver was identical or closely related to an isoform of hamster liver arginases.

Amino Acid Sequence↗

The CD46 transmembrane domain is required for efficient formation of measles-virus-mediated syncytium.

Two phosphatidylinositol (PI)-anchored versions of a measles virus (MV) receptor membrane cofactor protein (MCP; CD46) were generated by fusing the extracellular domain of MCP to the decay-accelerating factor (DAF; CD55) or its PI anchor. The PI-anchored forms of MCP expressed on Chinese hamster ovary cells, otherwise non-permissive to MV, conferred a smaller MV cytopathic effect than a wild-type MCP, a Ser/Thr-rich domain-deletion mutant and a cytoplasmic tail-deletion mutant of MCP. Therefore the differences in MV receptor properties between the two PI-anchored and three transmembrane forms were investigated. The PI-anchored forms were predominantly expressed on microvilli as in DAF, whereas the other transmembrane forms were found on intracellular membranes. The PI-anchored forms conferred high MV-binding capacity compared with the transmembrane versions. MV replication was, however, severely suppressed in cells expressing the PI-anchored forms, resulting in ineffective syncytium formation. In contrast, cell-to-cell fusion occurred efficiently after co-transfection of cDNA species encoding MV-H. MV-F and any version of MCP. Thus the PI-anchored forms, despite showing sufficient MV binding and cell-to-cell fusion competence together with MV-H and MV-F, mediate inefficient MV entry or replication, which causes severe suppression of the MV cytopathic effect. A biased receptor distribution on microvilli might participate in the selection of a low MV uptake pathway in the PI-anchored forms of MCP. Taken together, the transmembrane portion of MCP is a critical factor for effective virus-cell fusion and the subsequent MV replication.

Animals↗

Possible association of infertility with sperm-specific abnormality of CD46.

Three infertile patients fulfilling normal or subnormal criteria on routine semen analysis showed abnormal sperm CD46 (membrane cofactor protein of complement) by SDS-PAGE/immunoblotting analysis using a panel of monoclonal antibodies. The sperm CD46 isoform has been reported to be associated with sperm-egg interaction. These three patients expressed normal CD46 isoforms on their lymphocytes and granulocytes. Sperm-specific abnormalities in these proteins thus parallel male infertility, suggesting a new category of infertility, probably due to aberrations in the molecules related to sperm-egg interaction.

Acrosome↗

A novel protein that participates in nonself discrimination of malignant cells by homologous complement.

The human complement (C) system protects an individual against substances of nonself origin, including xenografts and microbial pathogens. Human cells express C-regulatory proteins, CD46 and CD55, thereby circumventing attack by C3, a major effector of C. Nevertheless, certain malignant cells, particularly those undergoing apoptotic stress, can activate homologous C, overcoming the regulatory actions of CD46 and/or CD55. The molecular mechanisms whereby malignant cells are tagged by homologous C3 remain largely unknown. We identified a novel gene product that converts human cells into targets for homologous complement. Only malignant cells and cell lines exposed to Fas or X-irradiation stimuli produced this protein, designated M161Ag, which was an unglycosylated 43-kDa protein. Analysis of cloned cDNAs indicated that this molecule was a secretory protein containing five amino acids encoded by TGA codons. Its functions were unique in that once secreted from the tumor cells, it bound back to the surface of these cells and activated homologous complement (C3) via the alternative pathway, allowing for C3 deposition on the membrane. This molecule may offer new insight into innate immunity; surveillance of tumor cells by complement is a common feature in the human immune system.

Amino Acid Sequence↗

Rapid purification of human complement receptor type 1 (CD35, CR1).

We established a rapid purification procedure for complement receptor type 1 (CR1, CD35). Human erythrocyte stromata were solubilized, and the extract was directly applied to a Red-Sepharose column. The eluate was diluted 2-fold, then subjected to an immunoaffinity column, anti-CR1 (named 31R)-conjugated to Sepharose. More than 50% of CR1 was recovered with purity of > 90%. The CR1 preparation showed sufficient cofactor activity for factor I as compared to that prepared by the conventional method. Since 31R recognizes a single epitope in CR1 including its rare variants and soluble forms, this method will allow us to recover with high efficiency these forms of CR1 which have been detected especially in some disease states.

Antibodies, Monoclonal↗

Mechanisms by which the surface expression of the glycosyl-phosphatidylinositol-anchored complement regulatory proteins decay-accelerating factor (CD55) and CD59 is lost in human leukaemia cell lines.

We have investigated the mechanisms of defects in the glycosyl-phosphatidylinositol (GPI)-anchored complement regulatory proteins delay-accelerating factor (DAF) and/or CD59 in a panel of human leukaemia cell lines that lack surface expression of these proteins: U937 (DAF+/CD59-), CEM (DAF-/CD59+), TALL (DAF-/CD59-) and a substrain of Ramos [Ramos(-)] (DAF-/CD59-). Northern blotting and reverse transcription-PCR revealed that the main cause of the DAF and/or CD59 deficiency is the failure of mRNA expression in most of the cell lines, except in Ramos(-) in which sufficient mRNA for DAF and CD59 was produced. U937, CEM and TALL cells were not defective in GPI anchor formation as assessed by the detection of other GPI-anchored proteins. No gene abnormality corresponding to DAF or CD59 was detected by Southern blotting. Thus the cause of the defects of DAF and/or CD59 in these leukaemia cell lines except for Ramos(-) is virtually undetectable steady-state levels of the relevant mRNA, most likely attributable to lack of transcription in these cell lines. On the other hand, Ramos(-) cells failed to generate a GPI anchor, whereas they normally expressed DAF and CD59 transcripts. The transfection of phosphatidylinositol-glycan class A (PIG-A) cDNA into Ramos(-) cells restored DAF and CD59 expression, indicating that the defective mechanism in GPI anchor formation is similar to that in paroxysmal noctural haemoglobinuria (PNH) cells, i.e. a deficiency of the PIG-A gene product. Thus the mechanisms of the defects of DAF and/or CD59 in human leukaemia cell lines are not uniform, and in most cases are different from that proposed to cause PNH.

Antigens, CD↗

Myoepithelial hamartoma of the small bowel: report of a case.

Benign small bowel tumors seldom cause symptoms, due to the fluid content and distensibility of the small bowel. We herein present the case of a solitary ileal hamartoma causing melena and abdominal pain in a 24-year-old man. The diagnosis of a submucosal ileal tumor was made after performing small bowel barium studies. Surgical treatment was undertaken, and a histological examination of the excised lesion, which showed a partially ulcerated tumor surface and extended from the submucosa to the subserosa, revealed numerous cystic glands of various sizes together with bundles of proliferating smooth muscle cells. Histochemical and immunohistochemical investigations were performed for differential diagnosis, and the tumor features were consistent with a diagnosis of ileal myoepithelial hamartoma. In the literature, small intestinal myoepithelial hamartomas are quite rare and this is the first report of a myoepithelial hamartoma causing melena.

Adult↗

The fertilizing ability of human epididymal sperm.

PURPOSE: Membrane cofactor protein (MCP), CD46, whose primary function is to protect host cells from homologous complement, has been presumed to serve as a sperm adhesion molecule for oocytes. The purpose of this study was to clarify the relationship between the properties of MCP expressed on epididymal sperm and their fertilizing ability in a recently developed strategy for assisted reproduction. METHODS: We collected ejaculated sperm from normal subjects and epididymal sperm from vasectomized subjects and patients with congenital absence of the vas deferens. Western blotting and cofactor activity assay were performed to investigated the structural and functional properties of MCP. RESULTS: Epididymal spermatozoa which showed a reduced fertilizing ability tended to react poorly with antibodies against MCP and also showed low cofactor activity, indicating weak complement regulatory activity compared to that of ejaculated spermatozoa. CONCLUSIONS: MCP is sufficiently expressed in ejaculated sperm in men with a normally developed epididymis but is diminished in epididymal sperm from men with congenital or acquired obstruction of the vas deferens.

Antigens, CD↗

Soluble CD46 (membrane cofactor protein, MCP) in human reproductive tract fluids.

CD46 (membrane cofactor protein, MCP) is a cell surface complement regulatory protein which may have an additional role in human sperm-egg interaction. A soluble form (sCD46) has also been detected in a number of biological fluids, most notably seminal plasma. The present study has employed a monoclonal antibody-based ELISA to assay sCD46 in reproductive tract fluids in normal and pathological conditions. Large amounts of sCD46 were detected in seminal plasma of both fertile and infertile men (combined mean, 4859 ng/ml). Vasectomized men had lower levels (mean, 2421 ng/ml), indicating contributory sources both before and after the vas deferens ligation site. Pre-colostrum also contained relatively high quantities (mean, 445 ng/ml), whereas breast milk (mean, 117 ng/ml), peritoneal fluid (mean, 154 ng/ml) and follicular fluid (mean, 107 ng/ml), as well as uterine (mean, 208 ng/ml), umbilical (mean, 166 ng/ml) and peripheral (mean, 206 ng/ml) blood plasma, had sCD46 levels within a comparable range. Amniotic fluid had low sCD46 concentrations (mean, 22 ng/ml). In endometriosis, peritoneal fluid levels of sCD46 were significantly raised (mean, 199 mg/ml). These results indicate distinctive fluid compartmentalisation of sCD46 consistent with a biological function in human reproductive tract fluids.

Amniotic Fluid↗

CD46, a complement regulatory protein/measles virus receptor, and its relation to hematological disorders.

During measles virus (MV) infection, lymphopenia and immune suppression are observed in humans, yet the mechanisms underlying these effects remain unknown except that membrane cofactor protein (MCP, CD46) acts as a receptor for MV, accelerating entry of the virus into host cells. CD46 is a complement regulator, the role of which is to protect host cells from the autologous complement system. Thus, it encompasses complement-related and MV-mediated immune modulation. In this review, I discuss the structural and functional differences between CD46 on lymphocytes and on granulocytes, which partly explain the higher susceptibility of lymphocytes to MV than other blood cells to clarify the mechanisms of MV-mediated lymphopenia and immune suppression, and help resolve the T cell immunity dysfunction secondary to virus infection including HIV.

Adult↗

C5b-8 step lysis of swine endothelial cells by human complement and functional feature of transfected CD59.

The authors established several swine endothelial cell (SEC) lines expressing human CD59 by transfection of cDNA, and assessed the function of the transfectant molecules in comparison with those of membrane cofactor protein (MCP) and decay-accelerating factor (DAF) in an in vitro hyperacute rejection model of swine to human discordant xenograft. At the usual expression rate, DAF and MCP protected SEC from human complement mediated cell lysis, but CD59 did not block human complement attack on SEC. However, CD59 protects SEC from cell lysis when sufficiently expressed as in human umbilical vein (HUVEC). The authors examined why CD59 needed so many molecules to protect human complement-mediated SEC lysis and found that SEC underwent lysis by human C5b-8. The degree of C5b-8 step lysis of SEC was approximately 70% of the total activation (C5b-9). Additionally, CD59 protected human complement activities less efficiently at the C5b-8 step than at the C9-step. Therefore, to overcome human complement mediated SEC lysis, C8 activity must be inhibited by dense expression of CD59.

Animals↗