ACTA HISTOCHEMICA ET CYTOCHEMICA
Online ISSN : 1347-5800
Print ISSN : 0044-5991
最新号
選択された号の論文の3件中1~3を表示しています
REVIEW
  • Igor Buchwalow, Jürgen Schnekenburger, Vera Samoilova, Werner Boecker, ...
    原稿種別: Review
    2018 年 51 巻 6 号 p. 167-172
    発行日: 2018/12/20
    公開日: 2018/12/20
    [早期公開] 公開日: 2018/11/03
    ジャーナル フリー HTML

    Nitric oxide (NO) is generated by a family of enzymes termed NO synthases (NOS) that convert L-arginine to NO and citrulline. The role of NO as an important biological mediator and recognition of the pathophysiological significance of superoxides/NO interaction has led to an intensive research and development of therapies based on the interception of the NO signaling cascade in the pancreatitis course. However, the presence and localization of the NO-generating enzymes in various organs including pancreas are subject to controversy. We assumed that this controversy might reflect rather the diversity of experimental approaches and an insufficient sensitivity of the methods used. Applying tyramide signal amplification (TSA) immunohistochemical technology, we were able detect all three NOS isoforms both in exocrine and endocrine compartments and in the vasculature in the normal pancreas and in pancreatitis. This also allowed us to demonstrate that oxidative stress runs ahead of NOS up-regulation, which implies that the NO enhancement in the course of pancreatitis is likely to be an adaptive mechanism aimed at maintaining the homeostatic cellular level of the bioactive NO. The aims of this minireview are to describe normal intrapancreatic NO pathways and the role of NO in the pancreatitis course.

REGULAR ARTICLE
  • Yuki Izawa, Karin Kashii-Magaribuchi, Kana Yoshida, Mayu Nosaka, Nanam ...
    原稿種別: Regular Article
    2018 年 51 巻 6 号 p. 173-183
    発行日: 2018/12/20
    公開日: 2018/12/20
    [早期公開] 公開日: 2018/12/15
    ジャーナル フリー HTML

    Vasculogenic mimicry (VM), referring to vasculogenic structures lined by tumor cells, can be distinguished from angiogenesis, and is responsible for the aggressiveness and metastatic potential of tumors. HCC1937/p53 cells were derived from triple-negative breast cancer (TNBC), and used to investigate the roles of breast cancer stem cells (CSCs) in the formation of VM. HCC1937/p53 cells formed mesh-like structures on matrigel culture in which expression of VM-related genes, vascular endothelial (VE)-cadherin, matrix metalloproteinase (MMP)-2 and MMP-9 was confirmed by droplet digital polymerase chain reaction (PCR). In immunofluorescence microscopy, aldehyde dehydrogenase (ALDH)1A3+ cells with properties of CSCs or progenitors and GATA binding protein 3 (GATA3)+ cells with more differentiated characteristics were localized in the bridging region and aggregated region of VM structures, respectively. In fluorescence-activated cell sorting analysis, ALDH+ cells, considered to be a subpopulation of CSCs sorted by the aldefluor assay, exhibited marked VM formation on matrigel in 24 hr, whereas ALDH cells did not form VM, indicating possible roles of CSCs in VM formation. The stem-like cancer cells resistant to p53-induced apoptosis, which expressed a high rate of ALDH1A3 and Sex-determining region Y (SRY)-box binding protein-2 (Sox-2), completed VM formation much faster than the control. These findings may provide clues to elucidate the significance of VM formed by treatment-resistant CSCs in the metastatic potential and poor prognosis associated with TNBC.

NOTE
  • Toshihiro Miyazaki, Tomomi T. Baba, Masako Mori, Toshihisa Komori
    原稿種別: Note
    2018 年 51 巻 6 号 p. 185-190
    発行日: 2018/12/20
    公開日: 2018/12/20
    [早期公開] 公開日: 2018/11/03
    ジャーナル フリー HTML

    We previously reported that the terminal differentiation of odontoblasts was inhibited in Runx2 transgenic {Tg(Col1a1-Runx2)} mice under the control of the 2.3-kb Col1a1 promoter. Odontoblasts in Tg(Col1a1-Runx2) mice lose their characteristic long cellular processes, and show marked reductions in the protein levels of markers for odontoblasts, such as dentin sialophosphoprotein, nestin, and microtubule-associated protein tau (Mapt). We herein demonstrated that collapsin response mediator protein 1 (CRMP1), a neuronal phosphoprotein that participates in various aspects of neuronal development, was specifically expressed in the differentiated odontoblasts of wild-type, but not Tg(Col1a1-Runx2) tooth germs by comparing expression profiles in wild-type and Tg(Col1a1-Runx2) mouse molars using microarray and immunohistochemical analyses. CRMP1 expression was detected at a slightly later differentiation stage in odontoblasts than type 1 collagen, nestin, and Mapt expression, which was observed from the onset of dentinogenesis. Among these proteins, CRMP1 was the most specifically localized in odontoblasts in the tooth germ. In erupted molars, odontoblast-specific CRMP1 expression decreased with age. These results indicate that CRMP1 is a novel marker protein for differentiated odontoblasts in mouse tooth germs, and suggest that CRMP1 participates in the morphogenesis of functioning odontoblasts.

feedback
Top