ACTA HISTOCHEMICA ET CYTOCHEMICA
Online ISSN : 1347-5800
Print ISSN : 0044-5991
ISSN-L : 0044-5991
Volume 50 , Issue 1
Showing 1-6 articles out of 6 articles from the selected issue
REGULAR ARTICLE
  • Hiroki Kameyama, Shinji Kudoh, Jun Hatakeyama, Akira Matuo, Takaaki It ...
    Type: Regular Article
    2017 Volume 50 Issue 1 Pages 1-9
    Published: February 28, 2017
    Released: February 28, 2017
    [Advance publication] Released: February 23, 2017
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    To study the significance of signal transducer and activator of transcription (Stat) 3 in lung epithelial development of fetal mice, we examined fetal mouse lungs, focusing on the expression of Clara cell secretory protein (CCSP), Forkhead box protein J1 (Foxj1), calcitonin gene-related peptide (CGRP), phosphorylated Stat3 (Tyr705), and hairy/enhancer of split (Hes) 1, and observed cultured fetal lungs upon treatment with IL-6, a Stat3 activator, or cucurbitacin I, a Stat3 inhibitor. Moreover, the interaction of Stat3 signaling and Hes1 was studied using Hes1 gene-deficient mice. Phosphorylated Stat3 was detected in fetal lungs and, immunohistochemically, phosphorylated Stat3 was found to be co-localized in developing Clara cells, but not in ciliated cells. In the organ culture studies, upon treatment with IL-6, quantitative RT-PCR revealed that CCSP mRNA increased with increasing Stat3 phosphorylation, while cucurbitacin I decreased Hes1, CCSP, Foxj1 and CGRP mRNAs with decreasing Stat3 phosphorylation. In the lungs of Hes1 gene-deficient mice, Stat3 phosphorylation was not markedly different from wild-type mice, the expression of CCSP and CGRP was enhanced, and the treatment of IL-6 or cucurbitacin I induced similar effects on mouse lung epithelial differentiation regardless of Hes1 expression status. Stat3 signaling acts in fetal mouse lung development, and seems to regulate Clara cell differentiation positively. Hes1 could regulate Clara cell differentiation in a manner independent from Stat3 signaling.

  • Abdulmajeed Al Drees, Mahmoud Salah Khalil, Mona Soliman
    Type: Regular Article
    2017 Volume 50 Issue 1 Pages 11-19
    Published: February 28, 2017
    Released: February 28, 2017
    [Advance publication] Released: February 22, 2017
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    Acute kidney failure is the main cause of death among patients with severe trauma due to massive blood loss and hemorrhagic shock (HS). Renal cell injury is caused by tissue ischemia. Renal ischemia initiates a complex and interconnected chain of events resulting in cell injury and renal cell necrosis. Nitric oxide plays a crucial role in renal function and can be inhibited by aminoguanidine (AG). We studied whether AG can ameliorate pathological renal changes associated with HS syndrome in a rat model and explored the AG protection mechanism. Rats were intraperitoneally injected with heparin sodium and mean arterial blood pressure was monitored. Animals were divided into three groups: control (without hemorrhage), with or without intra-arterially injected AG; HS (blood continuously withdrawn or reinfused to maintain an MABP of 35–40 mmHg); and HS with AG. We found that AG decreased plasma concentrations of urea, creatinine, and nitrates; ameliorated histological changes of HS-induced rats; and decreased the expressions of inducible nitrogen oxide synthase (iNOS), proapoptotic protein (BAX), and vitamin D receptors (VDR). AG ameliorated kidney injury by inhibiting iNOS resulting in decreased BAX and VDR expressions. Therefore, a therapeutic strategy targeting AG may provide new insights into kidney injury during severe shock.

  • Kazuyo Tsuchiya, Takuto Ikeda, Baatarsuren Batmunkh, Narantsog Choijoo ...
    Type: Regular Article
    2017 Volume 50 Issue 1 Pages 21-28
    Published: February 28, 2017
    Released: February 28, 2017
    [Advance publication] Released: February 22, 2017
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    Mucosal immune dysregulation associated with T cells plays a critical role in the development of inflammatory bowel diseases (IBD). However, the definite significances of these cells in IBD still remain unclear. Therefore, we investigated the population and expression of CD4+CD161+ T cells in the colonic lamina propria mononuclear cells (LPMCs) in patients with IBD by analyses using flow cytometry and immunohistochemistry. Interleukin-10 (IL-10) mRNA levels in both LPMCs and CD4+ T cells in lamina propria (LP-CD4+ T cells) were measured using a real-time quantitative reverse transcription-polymerase chain reaction. IL-10 production was investigated with immunohistochemistry. The results revealed that the population of CD4+CD161+ T cells was significantly decreased in active ulcerative colitis (UC) compared with inactive UC (P < 0.05). The CD4+CD161+ T cell population was inversely correlated with disease activity in patients with UC (r = −0.6326, P = 0.0055), but there was no significant correlation in those with Crohn’s disease. Over-expression of IL-10 mRNA in both LPMCs and LP-CD4+ T cells were detected in active UC. Immunohistochemistry revealed decreased frequency of CD161+ cells and increased IL-10 positive cells in active UC. The frequency of CD4+CD161+ T cells and IL-10 expression was supposed to be associated with the pathological status of mucosal immunoregulation in IBD.

  • Jun-Seok Lee, Hyun-Jin Kim, Chang-Hyun Ahn, Chang-Jin Jeon
    Type: Regular Article
    2017 Volume 50 Issue 1 Pages 29-37
    Published: February 28, 2017
    Released: February 28, 2017
    [Advance publication] Released: February 22, 2017
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    The direction selectivity of the retina is a distinct mechanism that is critical function of eyes for survival. The direction-selective retinal ganglion cells (DS RGCs) strongly respond to a preferred direction, but rarely respond to opposite direction or null directional visual stimuli. The DS RGCs are sensitive to acetylcholine, which is secreted from starburst amacrine cells (SACs) to the DS RGCs. Here, we investigated the existence and distribution of the nicotinic acetylcholine receptor (nAChR) α4 and β2 subunits on the dendritic arbors of the DS RGCs in adult rabbit retina using immunocytochemistry. The DS RGCs were injected with Lucifer yellow to identify their dendritic morphology. The double-labeled images of dendrites and nAChR subunits were visualized for reconstruction using high-resolution confocal microscopy. Although our results revealed that the distributional pattern of the nAChR subunits on the dendritic arbors of the DS RGCs was not asymmetric in the adult rabbit retina, the distribution of nAChR α4 and β2 subunits and molecular profiles of cholinergic inputs to DS RGCs in adult rabbit retina provide anatomical evidence for direction selectivity.

  • Baatarsuren Batmunkh, Narantsog Choijookhuu, Naparee Srisowanna, Uugan ...
    Type: Regular Article
    2017 Volume 50 Issue 1 Pages 39-48
    Published: February 28, 2017
    Released: February 28, 2017
    [Advance publication] Released: February 25, 2017
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    Although estrogen is implicated in the regulation of cell growth and differentiation in many organs, the exact mechanism for liver regeneration is not completely understood. We investigated the effect of estrogen on liver regeneration in male and female Wistar rats after 70% partial hepatectomy (PHx) and performed immunohistochemistry, western blotting and Southwestern histochemistry. 17β-estradiol (E2) and ICI 182,780 were injected into male rats on the day before PHx. The proliferating cell nuclear antigen (PCNA) labeling index reached a maximum at 48 hr after PHx in males, and at 36 hr in females and E2-treated male rats. Estrogen receptor α (ERα) was expressed in zones 1 and 2 in male rats, but was found in all zones in female rats. Interestingly, ERα was not detected at 6–12 hr after PHx but was found at 24–168 hr in male rats. However, ERα expression was found at all sampling time-points in female and E2-treated male rats. The activity of estrogen responsive element binding proteins was detected from 12 hr after PHx in male rats but was found from 6 hr in female and E2-treated male rats. ERα was co-expressed with PCNA during liver regeneration. These results indicate that estrogen may play an important role in liver regeneration through ERα.

  • Mingchun Yang, Hongkuan Yang, Hongpeng Guan, Tomoko Kato, Kenichi Muka ...
    Type: Regular Article
    2017 Volume 50 Issue 1 Pages 49-55
    Published: February 28, 2017
    Released: February 28, 2017
    [Advance publication] Released: February 23, 2017
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    Mitochondrial ferritin (FtMt) is a novel iron storage protein with high homology to H-ferritin. Unlike the ubiquitously expressed H- and L-ferritin, FtMt is expressed in specific tissues such as the testis, heart, and brain. The function of FtMt is not fully understood; however, evidence suggests that it has a neuroprotective role in neurodegenerative diseases. We have previously reported that FtMt is expressed in catecholaminergic neurons of the monkey brainstem. To explore FtMt expression in human dopaminergic neurons, we designed a novel monoclonal antibody, C65-2, directed against human FtMt. Here, we report the properties of our C65-2 antibody. Western blots analysis and immunoabsorption tests demonstrated that the C65-2 antibody specifically recognized FtMt with no cross-reactivity to H-ferritin. Immunohistochemistry showed that the C65-2 antibody detected FtMt in neurons of the substantia nigra pars compacta (SNc) in humans and monkeys. We confirmed that FtMt is expressed in dopaminergic neurons of the human SNc. Our results suggest that FtMt is involved in various physiological and pathological mechanisms in human dopaminergic neurons, and the C65-2 monoclonal antibody promises to be a useful tool for determining the localization and biological functions of FtMt in the brain.

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