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Eiichi Morii

Publications and source records attributed to Eiichi Morii.

24 records · Page 2Linked to original sources

Requirement of Gab2 for mast cell development and KitL/c-Kit signaling.

Mast cells are thought to participate in a variety of immune responses, such as parasite resistance and the allergic reaction. Mast cell development depends on stem cell factor (Kit ligand) and its receptor, c-Kit. Gab2 is an adaptor molecule containing a pleckstrin homology domain and potential binding sites for SH2 and SH3 domains. Gab2 is phosphorylated on tyrosine after stimulation with cytokines and growth factors, including KitL. Gab2-deficient mice were created to define the physiological requirement for Gab2 in KitL/c-Kit signaling and mast cell development. In Gab2-deficient mice, the number of mast cells was reduced markedly in the stomach and less severely in the skin. Bone marrow-derived mast cells (BMMCs) from the Gab2-deficient mice grew poorly in response to KitL. KitL-induced ERK MAP kinase and Akt activation were impaired in Gab2-deficient BMMCs. These data indicate that Gab2 is required for mast cell development and KitL/c-Kit signaling.

Adaptor Proteins, Signal Transducing↗

Isoforms of mi transcription factor preferentially expressed in cultured mast cells of mice.

MITF is a basic helix-loop-helix leucine zipper transcription factor, which is important for normal phenotypic expression of mast cells. Three isoforms of MITF have been known in mice, MITF-A, -H, and -M. Since cultured mast cells (CMCs) are useful for studying the function of MITF, we examined isoforms of MITF expressed in CMCs using 5'-RACE, and found a new isoform of MITF, MITF-E. We assessed the relative mRNA amount of various MITF isoforms with reverse transcription-PCR. When the mRNA amount of MITF-E was used as a standard, that of MITF-M was approximately 10%, that of MITF-H was approximately 1%, and that of MITF-A was approximately 0.1%. Although MITF-E was the preferential isoform in CMCs, peritoneal mast cells expressed only MITF-M. The expression profile of MITF isoforms appeared to be influenced by the developing process of mast cells.

3T3 Cells↗

Effect of MITF on mast cell differentiation.

The mi transcription factor (MITF) is a basic helix-loop-helix leucine zipper (bHLH-Zip) transcription factor and encoded by the mi locus of mice. Double gene dose of mutant allele at the mi locus results the decrease of mast cells and phenotypic abnormalities of mast cells. Various mutations have been reported at the mi locus. We divided them to null and inhibitory mutations. The tg is a typical null mutation due to the insertion of a transgene into the promoter region of MITF gene. Adult mice of tg/tg genotype can easily obtained and are a potentially useful tool for studying development and function of mast cells.

Animals↗

Regulation of mast cell phenotype by MITF.

The development of mast cells is controlled through the cooperative effects of growth factors and nuclear transcription factors. The signals generated by the binding of stem cell factor (SCF) to c-kit receptor tyrosine kinase (KIT) are essential for their development and survival. A double gene dose of mutant alleles at either the SCF or KIT locus results in a decrease of mast cells. A double gene dose of mutant alleles at the mi transcription factor (MITF) locus also results in mast cell deficiency. Although the phenotype of the few mast cells remaining in SCF and KIT mutant mice appeared to be normal, the phenotype of mast cells was abnormal in MITF mutant mice. We describe here the abnormalities of mast cells observed in MITF mutant mice.

Animals↗

Interaction and cooperation of mi transcription factor (MITF) and myc-associated zinc-finger protein-related factor (MAZR) for transcription of mouse mast cell protease 6 gene.

The mi transcription factor (MITF) is a basic-helix-loop-helix leucine zipper (bHLH-Zip) transcription factor that is important for the normal phenotypic expression of mast cells. Most transcription factors function in cooperation with other factors by protein-protein interactions. To search proteins interacting with MITF, we carried out a yeast two-hybrid screen and isolated Myc-associated zinc-finger protein related factor (MAZR) as a partner of MITF. When expressed with MITF in NIH/3T3 cells, MAZR was colocalized with MITF. The association of MAZR with MITF was further confirmed by a co-immunoprecipitation study and in vitro binding assay. The zinc-finger domain of MAZR and the Zip domain of MITF were essential for the interaction. MAZR was expressed in cultured mast cells and MST mastocytoma cells containing mouse mast cell protease (mMCP)-6 transcript abundantly. The overexpression of dominant negative MAZR in MST mastocytoma cells reduced the amount of mMCP-6 mRNA. The simultaneous transfection of MAZR and MITF significantly increased the promoter activity of the mMCP-6 gene, indicating that the MAZR and MITF synergistically transactivated the mMCP-6 gene. MAZR appeared to play important roles in the normal phenotypic expression of mast cells in association with MITF.

3T3 Cells↗

Embolic effects of superabsorbent polymer microspheres in rabbit renal model: comparison with tris-acryl gelatin microspheres and polyvinyl alcohol.

PURPOSE: We have developed a spherical embolic agent, superabsorbent polymer microspheres (SAP-MS). The aim of this study was to examine the embolic effects of SAP-MS in comparison with polyvinyl alcohol (PVA) particles and tris-acryl gelatin microsphere (Embosphere Microsphere; EM) in a rabbit renal model. MATERIALS AND METHODS: The right kidneys of nine rabbits were embolized with the given agents: PVA (180-300 microm) (n=3), EM (100-300 microm) (n=3), and SAP-MS (106-150 microm) (n=3). The embolized kidneys were evaluated by angiography and histology after one week. RESULTS: Renal artery occlusion and prominent coagulative necrosis were confirmed regardless of agent. PVA aggregated in the proximal vessels with tiny fragments migrating into glomeruli. Both EM and SAP-MS traveled distally up to the interlobular artery level, and a single particle achieved cross-sectional vessel occlusion. SAP-MS was markedly swollen, deformed, and conformed to the vessel lumen compared with the constantly spherical EM. Mild perivascular reaction was seen with both microspheres. CONCLUSION: SAP-MS resulted in targeted end-organ infarction in the rabbit renal model and showed different mechanical properties from other agents.

Acrylic Resins↗