巻号一覧
38 巻 (2005)
- 6 号 p. 347-
- 5 号 p. 295-
- 4 号 p. 253-
- 3 号 p. 185-
- 2 号 p. 87-
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38 巻, 2 号
選択された号の論文の8件中1～8を表示しています
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REVIEW
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Takeo Minematsu, Shunsuke Miyai, Masanori Suzuki, Michio Yamazaki, Sus ...2005 年 38 巻 2 号 p. 87-92
発行日: 2005年
公開日: 2005/05/20
ジャーナル フリーPituitary tumorigenesis is a complex pathway involving numerous factors and conditions, such as hormonal stimulations, cell cycle regulators, growth factors, and transcription factors. To better understand this disease, to date, several experimental animal models have been established and analyzed. This article reviews and updates the studies on molecular mechanisms of pituitary tumorigenesis which were investigated using experimental model animals.
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Yosky Kataoka, Yasuhisa Tamura, Yilong Cui, Hisao Yamada2005 年 38 巻 2 号 p. 93-98
発行日: 2005年
公開日: 2005/05/20
ジャーナル フリーIn recent years, studies on cell regeneration in the adult mammalian central nervous system have brought about the possibility of new strategies for treating neurological disorders. Many researchers have examined molecular/cellular-based approaches in vitro, while little has been determined about the modulatory processes affecting cellular proliferation and differentiation in vivo. We report here a new strategy to investigate cellular proliferation, differentiation, and regeneration using an experimental animal model for functional activation of the cerebral cortex in rats. The unilateral cerebral cortex was extensively activated by induction of cortical spreading depression (SD), characterized as propagation of neuronal/glial membrane depolarization. Cellular proliferation in the animals was assessed using histochemical studies with BrdU, an analog of thymidine. SD resulted in a dramatic increase in BrdU-labeled cells in the cortical hemisphere that had undergone the SD, depending on the number of elicited SD events. Immunohistochemical studies revealed that 53% of the BrdU-labeled cells in the SD-generated cortex were immunopositive for NG2, a maker of oligodendrocyte progenitor cells, while 25% were immunopositive for OX-42, a maker of microglia, at 3 days after SD. These studies indicate that neural activation induces cellular proliferation in the cerebral cortex, and that the cells subsequently differentiate into glial progenitors or microglia within 3 days.
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Hirokazu Ohtaki, Kenji Dohi, Tomoya Nakamachi, Sachiko Yofu, Sakura En ...2005 年 38 巻 2 号 p. 99-106
発行日: 2005年
公開日: 2005/05/20
ジャーナル フリーCerebrovascular disease is the third leading cause of death in the industrialized world and is also a major cause of long-lasting disability. The development of gene deficient and transgenic mice has recently aided in research into and development of specific surgical procedures for brain ischemia in mice. The models of brain ischemia are divided into global ischemia and focal ischemia. Global ischemia is divided into two sub-models, forebrain ischemia and total ischemia. Forebrain ischemia is widely used to analyze delayed neuronal cell death including apoptosis, while total ischemia is used to clarify the neuronal cell death by the systemic ischemia such as cardiac arrest. On the other hand, focal ischemia is used to analyze pathological stroke. Pathophysiology of brain ischemia has been clarified by the use of these models. This review outlines the pathways that lead to cell death following ischemia. Moreover, we have reviewed these currently-used mouse experimental models of global and focal ischemia.
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REGULAR ARTICLE
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Shunsuke Miyai, Johbu Itoh, Hanako Kajiya, Susumu Takekoshi, Robert Yo ...2005 年 38 巻 2 号 p. 107-114
発行日: 2005年
公開日: 2005/05/20
ジャーナル フリーRNA interference (RNAi) provides a powerful method for gene silencing in eukaryotic cells. We report on an RNAi technique-induced Pit-1 gene silencing in a GH-secreting cell line MtT/S using duplexes of 21-nt RNAs. By immunocytochemical analysis, the decrease in Pit-1 immunoreactivity was observed in a fraction of siRNA transfected MtT/S cells, while actin and tubulin showed no change in expression following transfection. Moreover, the double staining of Pit-1 and GH indicated that GH production was reduced only in MtT/S cells in which Pit-1 immunoreactivity was decreased by transfection. These results suggested that functional specific knock-down of Pit-1 was induced by transfection of siRNA. Together with the defects of somatotropic lineage and hypoplastic phenotypes in Snell dwarf mice and the transfection experiments using Pit-1 antisense oligonucleotides, our experiments support the theory that Pit-1 plays a crucial role in GH gene expression in individual cells.
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Kaoruko Nagai, Tsuyoshi Noguchi, Shozo Fujiwara, Katsunobu Kawahara, T ...2005 年 38 巻 2 号 p. 115-119
発行日: 2005年
公開日: 2005/05/20
ジャーナル フリーOur previous report illustrated that the epithelium of the human esophagus has numerous lymphocytes and Langerhans cells with Birbeck granules. In the present study, the distribution of Langerhans cells in the human esophagus was examined immunohistochemically. The human esophageal specimens were obtained by the surgery for esophageal carcinoma with informed consent. The tissue blocks were fixed with 10% formalin and embedded in paraffin. The thin sections were treated with anti-S-100 protein antibody, placed in IgG-gold (5 nm) solution as a second antibody, and then sensitized with the physical development method. The Langerhans cells, which showed a positive immunoreaction for the S-100, were distributed within the epithelium throughout the esophagus. Their distribution patterns differed according to the region of the esophagus. The Langerhans cells tended to increase in number as they moved further from the oral cavity toward the abdominal part. In this study, it was suggested that they played important roles in the immune response of the human esophagus.
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Takayoshi Yamaza, Satoya Mino, Ikiru Atsuta, Atsushi Danjo, Tadayoshi ...2005 年 38 巻 2 号 p. 121-129
発行日: 2005年
公開日: 2005/05/20
ジャーナル フリーThe junctional epithelium (JE) is a primary site of defense against periodontal pathogens. Cystatin C is an endogenous inhibitor of cysteine proteinases such as cathepsin B and also has antibacterial actions against periodontal pathogens. However, the distribution and role of cystatin C in JE have not been clarified. To investigate the function of cystatin C in the host defense at dentogingival junction, we examined the immunolocalization of cystatin C and cathepsin B in rat gingiva using light and electron microscopy. The JE (particularly the coronal portion) was immunopositive for cystatin C, and immunoelectron microscopy revealed that cystatin C was localized to the vesicular, granular, and vacuolar compartments of JE cells. The pattern of cathepsin B immunoreactivity in JE cells resembled that of cystatin C. Both cystatin C and cathepsin B appeared to be localized to endosomal/lysosomal compartments within JE cells. These findings suggest that cystatin C regulates cysteine proteinase activity and exerts antibacterial effects both in the lysosomal compartments of JE cells and in the intercellular spaces of the JE. Cystatin C is thus able to participate in host defense against periodontal pathogens at the dentogingival junction.
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Yoshihiro Akimoto, Koji Yamamoto, Eiji Munetomo, Lance Wells, Keith Vo ...2005 年 38 巻 2 号 p. 131-142
発行日: 2005年
公開日: 2005/05/20
ジャーナル フリーWe aimed to examine the changes of O-GlcNAc modification of proteins in diabetes, especially in the pathogenesis of diabetic complications. The expression of O-GlcNAc-modified proteins and O-GlcNAc transferase was examined by Western blot analysis and immunohistochemically in various tissues (sciatic nerve, kidney, retina, liver, skeletal muscle, white adipose tissue, skin) of diabetic Goto-Kakizaki (GK) rats and nondiabetic Wistar rats. In the diabetic GK rats the Western blot bands of sciatic nerve, kidney and liver increased in the intensity. In all of the tissues of the non-diabetic Wistar rats, the O-GlcNAc and O-GlcNAc transferase immunoreactivities were observed in almost all cells, with strong expression indicated in the nucleus and weak expression in the cytoplasm. In the diabetic GK rats, these immunoreactivities in the sciatic nerve, kidney, and liver increased in intensity. In these tissues, morphological abnormalities were also observed at both light and electron microscopic levels. In contrast, the Western blot bands and immunoreactivities in the other tissues did not change in the diabetic GK rats. Furthermore, no morphological changes were observed in these tissues. These results indicate that elevated O-GlcNAc modification of proteins may be involved in the diabetic complications seen in diabetic GK rats.
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Riko Kitazawa, Sohei Kitazawa2005 年 38 巻 2 号 p. 143-149
発行日: 2005年
公開日: 2005/05/20
ジャーナル フリーReceptor activator of NF-κB ligand (RANKL) has been identified as a prerequisite for osteoclastogenesis. To elucidate the molecular mechanism of osteolytic bone lesions, we investigated RANKL mRNA expression in mouse bone tissue from experimental models of mouse autoimmune arthritis and cancer associated osteolysis. Elbow joints of type II collagen-induced arthritis (CIA) mice and calvariae of mice transplanted with breast cancer cells under the scalp were fixed with 4% paraformaldehyde for 2 days, decalcified with 20% EDTA in phosphate buffer for 5 days and embedded in paraffin. For in situ hybridization, digoxigenin-labeled antisense (or sense) single-stranded DNA probes were prepared by unidirectional PCR using cDNA of mouse RANKL amplified by RT-PCR. In the articular lesions of CIA mice, TRAP-positive osteoclasts were found at eroded cartilage and bone as well as in the pannus. Synovial cells around these osteoclasts were strongly positive for RANKL, indicating that synovial cells contribute to osteoclastogenesis through authentic RANKL-RANK signaling. In the tumor-induced osteolytic lesions of the mouse calvaria, osteoblasts and stromal cells between the tumor foci and the bone surface expressed RANKL mRNA; osteoclastic bone resorption was observed adjacent to the RANKL-positive cells. Histological evaluation of RANKL expression in bone lesions is important, because osteoclasts and the RANKL-RANK system could be potential targets for therapeutic drugs in diseases with accelerated bone resorption.
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