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Volume 43 (2010)
- Issue 6 Pages 123-
- Issue 5 Pages 115-
- Issue 4 Pages 99-
- Issue 3 Pages 89-
- Issue 2 Pages 19-
- Issue 1 Pages 1-
Volume 43, Issue 6
Displaying 1-6 of 6 articles from this issue
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Song-Hee Yu, Yu-Jin Jang, Eun-Shil Lee, Dong-Youn Hwang, Chang-Jin Jeo ...2010 Volume 43 Issue 6 Pages 123-130
Published: 2010
Released on J-STAGE: December 29, 2010
Advance online publication: December 03, 2010JOURNAL FREE ACCESSAdipose derived stromal cells (ADSCs) were transplanted into a developing mouse eye to investigate the influence of a developing host micro environment on integration and differentiation. Green fluorescent protein-expressing ADSCs were transplanted by intraocular injections. The age of the mouse was in the range of 1 to 10 days postnatal (PN). Survival dates ranged from 7 to 28 post transplantation (DPT), at which time immunohistochemistry was performed. The transplanted ADSCs displayed some morphological differentiations in the host eye. Some cells expressed microtubule associated protein 2 (marker for mature neuron), or glial fibrillary acid protein (marker for glial cell). In addition, some cells integrated into the ganglion cell layer. The integration and differentiation of the transplanted ADSCs in the 5 and 10 PN 7 DPT were better than in the host eye the other age ranges. This study was aimed at demonstrating how the age of host micro environment would influence the differentiation and integration of the transplanted ADSCs. However, it was found that the integration and differentiation into the developing retina were very limited when compared with other stem cells, such as murine brain progenitor cell.
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Yoshinori Yamauchi, Eichi Tsuruga, Kazuki Nakashima, Yoshihiko Sawa, H ...2010 Volume 43 Issue 6 Pages 131-138
Published: 2010
Released on J-STAGE: December 29, 2010
Advance online publication: November 20, 2010JOURNAL FREE ACCESSElastic system fibers consist of microfibrils and tropoelastin. During development, microfibrils act as a template on which tropoelastin is deposited. Fibrillin-1 is the major component of microfibrils. It is not clear whether elastic fiber-associated molecules, such as fibulins, contribute to tropoelastin deposition. Among the fibulin family, fibulin-2, -4 and -5 are capable of binding to tropoelastin and fibrillin-1. In the present study, we used the RNA interference (RNAi) technique to establish individual gene-specific knockdown of fibulin-2, -4 and -5 in elastin-producing cells (human gingival fibroblasts; HGF). We then examined the extracellular deposition of tropoelastin using immunofluorescence. RNAi-mediated down-regulation of fibulin-4 and -5 was responsible for the diminution of tropoelastin deposition. Suppression of fibulin-5 appeared to inhibit the formation of fibrillin-1 microfibrils, while that of fibulin-4 did not. Similar results to those for HGF were obtained with human dermal fibroblasts. These results suggest that fibulin-4 and -5 may be associated in different ways with the extracellular deposition of tropoelastin during elastic fiber formation in elastin-producing cells in culture.
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Expression and Role of the BDNF Receptor-TrkB in Rat Adrenal Gland under Acute Immobilization StressYusuke Kondo, Juri Saruta, Masahiro To, Naoto Shiiki, Chikatoshi Sato, ...2010 Volume 43 Issue 6 Pages 139-147
Published: 2010
Released on J-STAGE: December 29, 2010
Advance online publication: December 03, 2010JOURNAL FREE ACCESSWe reported that plasma brain-derived neurotrophic factor (BDNF) was maximally elevated following a 60-min period of acute immobilization stress and that salivary glands were the main source of plasma BDNF under this stress condition. However, the expression pattern of the BDNF receptor, Tyrosine receptor kinase B (TrkB), under this condition has yet to be determined. We therefore investigated the effect of this stress on the expression level of TrkB in various rat organs using real-time PCR. No significant differences were found between controls and 60 min-stressed rats with respect to TrkB level in various organs. Only adrenal glands showed significantly increased TrkB mRNA levels after 60 min of stress. TrkB mRNA and protein were observed to localize in chromaffin cells. In addition, we investigated whether BDNF-TrkB interaction influences the release of stress hormones from PC12 cells, derived from chromaffin cells. Truncated receptor, TrkB-T1, was identified in PC12 cells using RT-PCR. Exposure of PC12 cells to BDNF induced the release of catecholamine. This BDNF-evoked release was totally blocked by administration of the K252a in which an inhibitor of Trk receptors. Thus, BDNF-TrkB interactions may modulate catecholamine release from adrenal chromaffin cells under acute stress conditions.
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Kyoko Itoh, Maki Mitani, Kunihiko Kawamoto, Naonobu Futamura, Itaru Fu ...2010 Volume 43 Issue 6 Pages 149-156
Published: 2010
Released on J-STAGE: December 29, 2010
Advance online publication: December 18, 2010JOURNAL FREE ACCESSMyotonic dystrophy (DM1) is known to be an adult-onset muscular dystrophy caused by the expansion of CTG repeats within the 3' untranslated region of the dystrophin myotonin protein kinase (DMPK) gene. The clinical features of DM1 include CNS symptoms, such as cognitive impairment and personality changes, the pathogenesis of which remains to be elucidated. We hypothesized that the distribution of neuropathological changes might be correlated with the extent of the length of the CTG repeats in the DMPK genes in DM1 patients. We studied the neuropathological changes in the brains of subjects with DM1 and investigated the extent of somatic instability in terms of CTG repeat expansion in the different brain regions of the same individuals by Southern blot analysis. The neuropathological changes included état criblé in the cerebral deep white matter and neurofibrillary tangles immunoreactive for phosphorylated tau in the hippocampus and entorhinal cortex, both of which were compatible with the subcortical dementia in DM1 patients. However, the length of the CTG repeats did not correlate with the regional differences in the extent of neuropathological changes. Our data suggested that pathomechanisms of dementia in DM1 might be more multifactorial rather than a toxic gain-of-function due to mutant RNA.
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Hiroaki Nakahara, Yoshihiro Konishi, Thomas G. Beach, Naoto Yamada, Sa ...2010 Volume 43 Issue 6 Pages 157-162
Published: 2010
Released on J-STAGE: December 29, 2010
Advance online publication: December 18, 2010JOURNAL FREE ACCESSWe and others have previously shown that reactive microglia express the major histocompatibility complex (MHC) class I and class II antigens in the hippocampus of patients suffering from epilepsy. Although the MHC glycoproteins serve as restriction elements for T lymphocytes, there is little information available regarding T lymphocytes in hippocampal sclerosis. In the present study, we investigated T lymphocyte infiltration in human hippocampi in four cases of epilepsy with hippocampal sclerosis, as well as in four control cases without neurological disease. No CD8- or CD4-positive T lymphocytes were seen in hippocampi from the control cases. In contrast, CD8- and CD4-positive T lymphocytes had infiltrated into the hippocampi of patients with hippocampal sclerosis. In addition, expression of intercellular adhesion molecule-1 was diffusely upregulated in the hippocampi with hippocampal sclerosis. These results indicate that T lymphocyte infiltration is involved in the pathology of hippocampal sclerosis.
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Morihiro Higashi, Jianyong Yu, Hiroshi Tsuchiya, Teruyoshi Saito, Tosh ...2010 Volume 43 Issue 6 Pages 163-168
Published: 2010
Released on J-STAGE: December 29, 2010
Advance online publication: December 23, 2010JOURNAL FREE ACCESSRho family G proteins including Rac regulate a variety of cellular functions, such as morphology, motility, and gene expression. Here we developed a fluorescence resonance energy transfer-based analysis in which we could monitor the activity of Rac1. To detect fluorescence resonance energy transfer, yellow fluorescent protein fused Rac1 and cyan fluorescent protein fused Cdc42-Rac1-interaction-binding domain of Pak1 protein were used as intermolecular probes of FRET. The fluorophores were separated with linear unmixing method. The fluorescence resonance energy transfer efficiency was measured by acceptor photobleaching assisted assay. With these methods, the Rac1 activity was visualized in a cell. The present findings indicate that this approach is sensitive enough to achieve results similar to those from ratiometric fluorescence resonance energy transfer analysis.
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