Cell Biology: State of the Art and Perspectives in Japan

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (15 June 2023) | Viewed by 15199

Special Issue Editors


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Guest Editor
Research Institute of Odontology (M-RIO), School of Dentistry, Meikai University, Sakado 350-0283, Japan
Interests: apoptosis; NAD+ metabolism; poly(ADP-ribosyl)ation; post-translational modification; DNA replication; DNA repair; carcinogenesis; warburg effect; neuro-inflammation; neuronal disorders; aging; transcription regulation; in silico drug design; AI medicine; anti-cancer drug; anti-inflammatory drug

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Guest Editor
Laboratory for Zero-Carbon Energy, Tokyo Institute of Technology, Institute of Innovative Research, N1-30 2-12-1 Ookayama, Meguro-ku, Tokyo 152-8550, Japan
Interests: radiation; biological effects of radiation; biological response to radiation in molecular terms; hyperthermia; cancer radiation therapy

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Guest Editor
1. Department of Molecular and Genomic Biomedicine, Center for Bioinformatics and Molecular Medicine, Nagasaki University Graduate School of Biomedical Sciences, 1-12-4 Sakamoto, Nagasaki 852-8523, Japan
2. Visiting Scientist, Central Radioisotope Division, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan
Interests: radiation oncology; biology in anti-cancer treatment; polyADP-ribosylation; anti-tumor therapeutic; mouse; boron neutron capture therapy
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
1. Radiation Oncology, University Hospital Essen, University Duisburg, Strahlenklinik, Hufeland Street 55, 45122 Essen, Germany
2. Neutron Therapy Research Center, Okayama University, Okayama 700-8530, Japan
3. German Society for Boron Neutron Capture Therapy, 45122 Essen, Germany
Interests: radiation oncology; hadron therapy; boron neutron capture therapy (BNCT); neutrons; high-LET radiation; radiation biology; eye tumors; ophthalmic oncology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to provide a comprehensive overview of the state of the art of cell biology in Japan. We invite research papers that will consolidate our understanding of this area. The Special Issue will publish full research articles and comprehensive reviews. Potential topics include, but are not limited to, the following research areas: 

  • Cell structure: organelles, cytoskeleton, cell membrane, capsule, flagella, etc.;
  • Cell physiology: cell growth, protein synthesis, division, movement of proteins, active/passive transport, intra- and extracellular signaling, adhesion, DNA repair, etc.;
  • Cellular metabolism: adaptive metabolism, metabolism and intracellular trafficking, immunometabolism, metabolic disorder, etc.;
  • Cell movement and motility: membrane trafficking, cell division, cell migration, etc.;
  • Cell techniques: cell and tissue culture, isolation, and fractionation of cells, immunocytochemistry (ICC), in situ hybridization (ISH), transfection, and optogenetics;
  • Omics: transcriptomics, genomics, proteomics, metabolomics, glycomics, lipidomics, interactomics, fluxomics, and biomics;
  • Autophagy and apoptosis;
  • Cell aging and death;
  • Cell growth and differentiation;
  • Stem cells;
  • Genetic disorders;
  • Plant, algae, and fungi cell biology;
  • Immune cell research;
  • Radiation effects on cells.

This Special Issue also makes it possible to provide a comprehensive overview of your laboratory's research efforts in recent years and to outline prospects for the future. We look forward to reading your contributions.

Prof. Dr. Sei-ichi Tanuma
Dr. Yoshihisa Matsumoto
Dr. Mitsuko Masutani
Prof. Dr. Wolfgang Sauerwein
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (7 papers)

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Research

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13 pages, 2491 KiB  
Article
Calmodulin as a Key Regulator of Exosomal Signal Peptides
by Kenji Ono, Mikio Niwa, Hiromi Suzuki, Nahoko Bailey Kobayashi, Tetsuhiko Yoshida and Makoto Sawada
Cells 2023, 12(1), 158; https://doi.org/10.3390/cells12010158 - 30 Dec 2022
Cited by 2 | Viewed by 1511
Abstract
Signal peptides (SPs) and their fragments play important roles as biomarkers and substances with physiological functions in extracellular fluid. We previously reported that SP fragments were released into extracellular fluid via exosomes and bound to calmodulin (CaM), an exosomal component, in a cell-free [...] Read more.
Signal peptides (SPs) and their fragments play important roles as biomarkers and substances with physiological functions in extracellular fluid. We previously reported that SP fragments were released into extracellular fluid via exosomes and bound to calmodulin (CaM), an exosomal component, in a cell-free system. However, it currently remains unclear whether CaM intracellularly interacts with SP fragments or is involved in the trafficking of these fragments to exosomes. Therefore, the present study examined the binding of CaM to SP fragments in T-REx AspALP cells, transformed HEK293 cells expressing amyloid precursor protein (APP) SP flanking a reporter protein, and their exosomes. APP SP fragments were detected in exosomes from T-REx AspALP cells in the absence of W13, a CaM inhibitor, but were present in lower amounts in exosomes from W13-treated cells. Cargo proteins, such as Alix, CD63, and CD81, were increased in W13-treated T-REx AspALP cells but were decreased in their exosomes. Furthermore, CaM interacted with heat shock protein 70 and CD81 in T-REx AspALP cells and this increased in the presence of W13. APP SP fragments were detected in intracellular CaM complexes in the absence of W13, but not in its presence. These results indicate that CaM functions as a key regulator of the transport of SP fragments into exosomes and plays novel roles in the sorting of contents during exosomal biogenesis. Full article
(This article belongs to the Special Issue Cell Biology: State of the Art and Perspectives in Japan)
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21 pages, 3451 KiB  
Article
Two Distinct Mechanisms Underlying γδ T Cell-Mediated Regulation of Collagen Type I in Lung Fibroblasts
by Daisuke Okuno, Noriho Sakamoto, Yoshiko Akiyama, Takatomo Tokito, Atsuko Hara, Takashi Kido, Hiroshi Ishimoto, Yuji Ishimatsu, Mohammed S. O. Tagod, Haruki Okamura, Yoshimasa Tanaka and Hiroshi Mukae
Cells 2022, 11(18), 2816; https://doi.org/10.3390/cells11182816 - 09 Sep 2022
Viewed by 2140
Abstract
Idiopathic pulmonary fibrosis is a chronic intractable lung disease, leading to respiratory failure and death. Although anti-fibrotic agents delay disease progression, they are not considered curative treatments, and alternative modalities have attracted attention. We examined the effect of human γδ T cells on [...] Read more.
Idiopathic pulmonary fibrosis is a chronic intractable lung disease, leading to respiratory failure and death. Although anti-fibrotic agents delay disease progression, they are not considered curative treatments, and alternative modalities have attracted attention. We examined the effect of human γδ T cells on collagen type I in lung fibroblasts. Collagen type I was markedly reduced in a γδ T cell number-dependent manner following treatment with γδ T cells expanded with tetrakis-pivaloxymethyl 2-(thiazole-2-ylamino) ethylidene-1,1-bisphosphonate (PTA) and interleukin-2. Collagen type I levels remained unchanged on addition of γδ T cells to the culture system through a trans-well culture membrane, suggesting that cell–cell contact is essential for reducing its levels in lung fibroblasts. Re-stimulating γδ T cells with (E)-4-hydroxy-3-methylbut-2-enyl diphosphate (HMBPP) reduced collagen type I levels without cell–cell contact, indicating the existence of HMBPP-induced soluble anti-fibrotic factors in γδ T cells. Adding anti-interferon-γ (IFN-γ)-neutralizing mAb restored collagen type I levels, demonstrating that human γδ T cell-derived IFN-γ reduces collagen type I levels. Conversely, interleukin-18 augmented γδ T cell-induced suppression of collagen type I. Therefore, human γδ T cells reduce collagen levels in lung fibroblasts via two distinct mechanisms; adoptive γδ T cell transfer is potentially a new therapeutic candidate. Full article
(This article belongs to the Special Issue Cell Biology: State of the Art and Perspectives in Japan)
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Review

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16 pages, 3014 KiB  
Review
Functional Diversity of Novel Lectins with Unique Structural Features in Marine Animals
by Tomomitsu Hatakeyama and Hideaki Unno
Cells 2023, 12(14), 1814; https://doi.org/10.3390/cells12141814 - 09 Jul 2023
Cited by 2 | Viewed by 1035
Abstract
Due to their remarkable structural diversity, glycans play important roles as recognition molecules on cell surfaces of living organisms. Carbohydrates exist in numerous isomeric forms and can adopt diverse structures through various branching patterns. Despite their relatively small molecular weights, they exhibit extensive [...] Read more.
Due to their remarkable structural diversity, glycans play important roles as recognition molecules on cell surfaces of living organisms. Carbohydrates exist in numerous isomeric forms and can adopt diverse structures through various branching patterns. Despite their relatively small molecular weights, they exhibit extensive structural diversity. On the other hand, lectins, also known as carbohydrate-binding proteins, not only recognize and bind to the diverse structures of glycans but also induce various biological reactions based on structural differences. Initially discovered as hemagglutinins in plant seeds, lectins have been found to play significant roles in cell recognition processes in higher vertebrates. However, our understanding of lectins in marine animals, particularly marine invertebrates, remains limited. Recent studies have revealed that marine animals possess novel lectins with unique structures and glycan recognition mechanisms not observed in known lectins. Of particular interest is their role as pattern recognition molecules in the innate immune system, where they recognize the glycan structures of pathogens. Furthermore, lectins serve as toxins for self-defense against foreign enemies. Recent discoveries have identified various pore-forming proteins containing lectin domains in fish venoms and skins. These proteins utilize lectin domains to bind target cells, triggering oligomerization and pore formation in the cell membrane. These findings have spurred research into the new functions of lectins and lectin domains. In this review, we present recent findings on the diverse structures and functions of lectins in marine animals. Full article
(This article belongs to the Special Issue Cell Biology: State of the Art and Perspectives in Japan)
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21 pages, 2642 KiB  
Review
The Pursuit of the “Inside” of the Amyloid Hypothesis—Is C99 a Promising Therapeutic Target for Alzheimer’s Disease?
by Nobumasa Takasugi, Masato Komai, Nanaka Kaneshiro, Atsuya Ikeda, Yuji Kamikubo and Takashi Uehara
Cells 2023, 12(3), 454; https://doi.org/10.3390/cells12030454 - 31 Jan 2023
Cited by 3 | Viewed by 2386
Abstract
Aducanumab, co-developed by Eisai (Japan) and Biogen (U.S.), has received Food and Drug Administration approval for treating Alzheimer’s disease (AD). In addition, its successor antibody, lecanemab, has been approved. These antibodies target the aggregated form of the small peptide, amyloid-β (Aβ), which accumulates [...] Read more.
Aducanumab, co-developed by Eisai (Japan) and Biogen (U.S.), has received Food and Drug Administration approval for treating Alzheimer’s disease (AD). In addition, its successor antibody, lecanemab, has been approved. These antibodies target the aggregated form of the small peptide, amyloid-β (Aβ), which accumulates in the patient brain. The “amyloid hypothesis” based therapy that places the aggregation and toxicity of Aβ at the center of the etiology is about to be realized. However, the effects of immunotherapy are still limited, suggesting the need to reconsider this hypothesis. Aβ is produced from a type-I transmembrane protein, Aβ precursor protein (APP). One of the APP metabolites, the 99-amino acids C-terminal fragment (C99, also called βCTF), is a direct precursor of Aβ and accumulates in the AD patient’s brain to demonstrate toxicity independent of Aβ. Conventional drug discovery strategies have focused on Aβ toxicity on the “outside” of the neuron, but C99 accumulation might explain the toxicity on the “inside” of the neuron, which was overlooked in the hypothesis. Furthermore, the common region of C99 and Aβ is a promising target for multifunctional AD drugs. This review aimed to outline the nature, metabolism, and impact of C99 on AD pathogenesis and discuss whether it could be a therapeutic target complementing the amyloid hypothesis. Full article
(This article belongs to the Special Issue Cell Biology: State of the Art and Perspectives in Japan)
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17 pages, 1079 KiB  
Review
The Role of the Plasminogen/Plasmin System in Inflammation of the Oral Cavity
by Tetiana Yatsenko, Maksym Skrypnyk, Olga Troyanovska, Morikuni Tobita, Taro Osada, Satoshi Takahashi, Koichi Hattori and Beate Heissig
Cells 2023, 12(3), 445; https://doi.org/10.3390/cells12030445 - 30 Jan 2023
Cited by 7 | Viewed by 3284
Abstract
The oral cavity is a unique environment that consists of teeth surrounded by periodontal tissues, oral mucosae with minor salivary glands, and terminal parts of major salivary glands that open into the oral cavity. The cavity is constantly exposed to viral and microbial [...] Read more.
The oral cavity is a unique environment that consists of teeth surrounded by periodontal tissues, oral mucosae with minor salivary glands, and terminal parts of major salivary glands that open into the oral cavity. The cavity is constantly exposed to viral and microbial pathogens. Recent studies indicate that components of the plasminogen (Plg)/plasmin (Pm) system are expressed in tissues of the oral cavity, such as the salivary gland, and contribute to microbial infection and inflammation, such as periodontitis. The Plg/Pm system fulfills two major functions: (a) the destruction of fibrin deposits in the bloodstream or damaged tissues, a process called fibrinolysis, and (b) non-fibrinolytic actions that include the proteolytic modulation of proteins. One can observe both functions during inflammation. The virus that causes the coronavirus disease 2019 (COVID-19) exploits the fibrinolytic and non-fibrinolytic functions of the Plg/Pm system in the oral cavity. During COVID-19, well-established coagulopathy with the development of microthrombi requires constant activation of the fibrinolytic function. Furthermore, viral entry is modulated by receptors such as TMPRSS2, which is necessary in the oral cavity, leading to a derailed immune response that peaks in cytokine storm syndrome. This paper outlines the significance of the Plg/Pm system for infectious and inflammatory diseases that start in the oral cavity. Full article
(This article belongs to the Special Issue Cell Biology: State of the Art and Perspectives in Japan)
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17 pages, 2066 KiB  
Review
Novel Roles of Nanog in Cancer Cells and Their Extracellular Vesicles
by Mikako Saito
Cells 2022, 11(23), 3881; https://doi.org/10.3390/cells11233881 - 01 Dec 2022
Cited by 3 | Viewed by 2078
Abstract
The use of extracellular vesicle (EV)-based vaccines is a strategically promising way to prevent cancer metastasis. The effective roles of immune cell-derived EVs have been well understood in the literature. In the present paper, we focus on cancer cell-derived EVs to enforce, more [...] Read more.
The use of extracellular vesicle (EV)-based vaccines is a strategically promising way to prevent cancer metastasis. The effective roles of immune cell-derived EVs have been well understood in the literature. In the present paper, we focus on cancer cell-derived EVs to enforce, more thoroughly, the use of EV-based vaccines against unexpected malignant cells that might appear in poor prognostic patients. As a model of such a cancer cell with high malignancy, Nanog-overexpressing melanoma cell lines were developed. As expected, Nanog overexpression enhanced the metastatic potential of melanomas. Against our expectations, a fantastic finding was obtained that determined that EVs derived from Nanog-overexpressing melanomas exhibited a metastasis-suppressive effect. This is considered to be a novel role for Nanog in regulating the property of cancer cell-derived EVs. Stimulated by this result, the review of Nanog’s roles in various cancer cells and their EVs has been updated once again. Although there was no other case presenting a similar contribution by Nanog, only one case suggested that NANOG and SOX might be better prognosis markers in head and neck squamous cell carcinomas. This review clarifies the varieties of Nanog-dependent phenomena and the relevant signaling factors. The information summarized in this study is, thus, suggestive enough to generate novel ideas for the construction of an EV-based versatile vaccine platform against cancer metastasis. Full article
(This article belongs to the Special Issue Cell Biology: State of the Art and Perspectives in Japan)
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7 pages, 1695 KiB  
Commentary
Molecular Regulation of Autophagy and Asymmetric Cell Division by Cancer Stem Cell Marker CD133
by Hideki Izumi, Yasuhiko Kaneko and Akira Nakagawara
Cells 2023, 12(5), 819; https://doi.org/10.3390/cells12050819 - 06 Mar 2023
Cited by 2 | Viewed by 1696
Abstract
CD133, also called prominin-1, is widely known as a cancer stem cell marker, and its high expression correlates with a poor prognosis in many cancers. CD133 was originally discovered as a plasma membranous protein in stem/progenitor cells. It is now known that Src [...] Read more.
CD133, also called prominin-1, is widely known as a cancer stem cell marker, and its high expression correlates with a poor prognosis in many cancers. CD133 was originally discovered as a plasma membranous protein in stem/progenitor cells. It is now known that Src family kinases phosphorylate the C-terminal of CD133. However, when Src kinase activity is low, CD133 is not phosphorylated by Src and is preferentially downregulated into cells through endocytosis. Endosomal CD133 then associates with HDAC6, thereby recruiting it to the centrosome via dynein motors. Thus, CD133 protein is now known to localize to the centrosome as endosomes as well as to the plasma membrane. More recently, a mechanism to explain the involvement of CD133 endosomes in asymmetric cell division was reported. Here, we would like to introduce the relationship between autophagy regulation and asymmetric cell division mediated by CD133 endosomes. Full article
(This article belongs to the Special Issue Cell Biology: State of the Art and Perspectives in Japan)
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