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Volume 37 (2004)
- Issue 6 Pages 331-
- Issue 5 Pages 281-
- Issue 4 Pages 223-
- Issue 3 Pages 153-
- Issue 2 Pages 65-
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Volume 37, Issue 3
Displaying 1-7 of 7 articles from this issue
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REVIEW
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Akira Matsuno, Tadashi Nagashima2004 Volume 37 Issue 3 Pages 153-158
Published: 2004
Released on J-STAGE: July 14, 2004
JOURNAL FREE ACCESSPaclitaxel, one of the antimicrotubule drugs, can suppress the growth of C6 glioma cells. However, paclitaxel may also accelerate in vitro locomotion of glioma cells. Another choice of antimicrotubule drugs is estramustine which has cytotoxic effects in human and rat glioma cells. We verified the role of microtubule-associated protein (MAP) 1A in proliferation of rat C6 glioma cells. We confirmed that the in vitro and in vivo suppression of MAP 1A using antisense synthetic phosphorothioate oligonucleotide can inhibit the proliferation of rat C6 glioma cells and may thus serve as a novel antisense therapy for glioma. It is noteworthy that the therapies targeting microtubules and MAPs, especially those using antisense strategy, are useful antitumor therapies for gliomas.
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REGULAR ARTICLE
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Hideho Ueda, Hideo Tezuka, Akinori Nakamura2004 Volume 37 Issue 3 Pages 159-162
Published: 2004
Released on J-STAGE: July 14, 2004
JOURNAL FREE ACCESSIt has been thought that the wasted mouse is a good model for motor neuron disease. Recently, it was found that the wasted mouse is caused by a gene defect of elongation factor 1α2, but the mechanism of the abnormal phenotype remains poorly understood. In the present study, we examined spinal motor neurons of wasted mice with light and electron microscopy. Confocal images with lamin B immunolabeling and conventional electron micrographs demonstrate that nuclear envelope breakdown (NEB) is a prominent feature of large motor neurons in wasted mice, although probable intercalated neurons or glial cells show no abnormalities. Furthermore, motor neuron death in wasted mice seems to be neither apoptosis nor necrosis. These data suggest that to understand the mechanism about NEB of the spinal motor neuron in wasted mice could shed light on certain motor neuron diseases.
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Liying Su, Kazuhisa Hasui, Kazunobu Sueyoshi, Sachie Matsushita, Shini ...2004 Volume 37 Issue 3 Pages 163-172
Published: 2004
Released on J-STAGE: July 14, 2004
JOURNAL FREE ACCESSTo study human gastric epithelial development, we examined the expression of MUC1 core, sialylated MUC1, MUC2, MUC5AC, and MUC6 in the stomachs of 22 fetuses at 9 to 30 weeks' gestation and of 7 neonates. Fetal gastric epithelial development was divided from the literature into the first stage of primitive gastric epithelial stem cells showing a columnar appearance, the second stage of primitive gastric stem cells forming primitive glands, and the third stage of gastric stem cells differentiating to fundic and pyloric glandular cells. Primitive gastric epithelial stem cells expressed MUC1 core and sialylated MUC1, and developed into early primitive gastric stem cells expressing MUC5AC. The primitive gastric stem cells and the gastric stem cells expressed the mucins examined. In the third stage, expression of the mucins was suppressed once, but the gastric glandular cells again expressed MUC1 core and sialylated MUC1, MUC2, and MUC6 in neonates, whereas most of the epithelial cells expressed MUC5AC. This suggests the postnatal maturation of the gastric glandular cells. Developing gastric stem cells expressed the mucins examined, with the simultaneous expression of MUC1 core and sialylated MUC1 in these gastric stem cells suggesting the high production and incomplete glycosylation of MUC1, and MUC5AC expression being involved in early gastric organogenesis.
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Yuji Moriwaki, Sumio Takahashi, Zenta Tsutsumi, Tsuneyoshi Ka, Toshika ...2004 Volume 37 Issue 3 Pages 173-182
Published: 2004
Released on J-STAGE: July 14, 2004
JOURNAL FREE ACCESSThe localization of adenosine deaminase (ADA 1) in human tissues was investigated by an immunohistochemical method. Tissues were taken from cadavers, fixed with 4% paraformaldehyde-PBS, and embedded in paraffin, and then examined following immunoperoxidase staining using a rabbit polyclonal antibody against keyhole limpet hemocyanin (KLH)-peptide conjugate (Ser-Phe-Leu-Pro-Glu-Asp-Glu-Lys-Arg-Glu-Leu-Leu) constructed from a human adenosine deaminase cDNA sequence. Immunohistochemical analysis demonstrated that ADA 1 was distributed in various human tissues, with intense reactivity observed in surface epithelia of the esophagus, stomach, small intestine, renal tubules, glandular cells of the small intestine, endothelial lining cells of the liver, and alveoli of the lung. Moderate reactivity was observed in the glomerulus cells of the kidney, epithelia and glandular cells of the large intestine, and hepatic parenchymal cells. This ubiquitous but cell-specific localization suggests that ADA 1 plays an important role in selected cells through the degradation of adenosine, a pharmacological active nucleoside.
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Guangjun Li, Toshihiro Kobayashi, Shohko Tsunawaki, Yasuhiro Ogawa, Ha ...2004 Volume 37 Issue 3 Pages 183-189
Published: 2004
Released on J-STAGE: July 14, 2004
JOURNAL FREE ACCESSFungal gliotoxin (GTX) is known to possess several potent biological effects such as immunosuppression and apoptosis. The function of this toxin, however, remains to be established. Herein we focused on the effects of GTX on the NADPH oxidase system, which includes the production of superoxide (O2-) and the exocytosis of the oxidant-producing intracellular compartments (OPIC), in human neutrophils stimulated with phorbol myristate acetate (PMA). Biochemical analyses indicated that GTX inhibits both the extracellular release of O2- and the intracellular production of the oxidant generated upon activation of the NADPH oxidase complex, and that the toxin suppresses the up-regulation to the cell surface of alkaline phosphatase activity which is a marker enzyme of OPIC. Fluorescence as well as enzyme cytochemical studies showed that O2- is produced in intracellular compartments in PMA-stimulated cells, but not in the stimulated cells exposed to GTX. Moreover, electron microscopy revealed that GTX inhibits the association of OPIC with the plasma membrane. Taken together, the present findings confirmed that GTX inhibits the extracellular release of O2- and the intracellular production of the oxidant, and first demonstrate that the toxin suppresses the exocytosis of OPIC in human neutrophils stimulated with PMA.
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Shigeko Fushimi, Yoshihiro Konishi, Teruo Shirabe2004 Volume 37 Issue 3 Pages 191-204
Published: 2004
Released on J-STAGE: July 14, 2004
JOURNAL FREE ACCESSWe investigated the cellular and subcellular localization of IGF-II receptors in the adult mouse central nervous system (CNS). The IGF-II receptor and the cation-independent (CI) mannose-6-phosphate (M6P) receptor are identical. Immunohistochemistry demonstrated that IGF-II/CI-M6P receptor immunoreactivity was mostly restricted to middle- to large-sized neurons throughout the CNS. A small number of glial cells were weakly to moderately labeled. IGF-II/CI-M6P receptor immunoreactivity was largely recognized within endosome-lysosomal structures in the neurons by immuno-electron microscopy (EM) of the CNS tissues. More intense labeling was observed in larger neurons that included more abundant endosome-lysosomal structures, indicating that IGF-II/CI-M6P receptor immunoreactivity reflects the endosome-lysosomal activity specifically present in neurons. These results are consistent with the general assumption that IGF-II/CI-M6P receptors are involved in sorting lysosomal enzymes within cells. IGF-II/CI-M6P receptors also endocytose secreted IGF-II and M6P-containing glycoproteins as scavenger receptors. Furthermore, it has been reported that they are involved in the development of transmembrane IGF-II signals. Therefore, we next tried to determine if they are expressed on the cell surface of primary cultured cortical neurons. By immunofluorescence and immuno-EM, particularly by immuno-scanning EM, expression of IGF-II/CI-M6P receptors was demonstrated in the neuronal cell surface in response to IGF-II treatment.
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Wuxiong Zhou, Masahito Oyamada, Yumiko Oyamada, Tetsuro Takamatsu2004 Volume 37 Issue 3 Pages 205-215
Published: 2004
Released on J-STAGE: July 14, 2004
JOURNAL FREE ACCESSAlthough gap junctions are thought to play an important role in moderating apoptosis, the basic phenomena underlying when and where the alterations of gap junctions occur during apoptosis have not been well documented. In this study we analyzed the spatiotemporal changes of connexin (Cx) during UV light-induced apoptosis using Cx43-enhanced green fluorescent protein (EGFP)-expressing HeLa cells, and compared them with those of mitochondrial membrane potential (MMP) using tetramethylrhodamine ethyl ester (TMRE) and nuclear morphological observation using Hoechst 33342. At 2 hr post-UV-irradiation, a third of the cells were TMRE negative, i.e., they showed the loss of MMP, but with slight nuclear fragmentation, and high percentages of linear Cx43-EGFP plaques were found among both TMRE-positive and TMRE-negative cells. At 4 hr post-UV-irradiation, the percentage of these linear plaques was decreased, and both punctate and diffuse localization of Cx43-EGFP were noted in the cytoplasm of TMRE-negative cells without nuclear fragmentation. At 8 hr post-irradiation, punctate cytoplasmic localization of Cx43-EGFP was noted in TMRE-negative cells with nuclear fragmentation. Treatment with the caspase inhibitor Z-VAD-FMK blocked nuclear fragmentation and partially preserved both gap junctional plaques and MMP. These results indicate that, during apoptosis, Cx mobilization into the cytoplasm occurs after MMP depolarization but before nuclear fragmentation and that this alteration partly depends on caspase.
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