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  1. Article: Adjuvant Activity of Synthetic Lipid A of

    Wang, Yunru / Hosomi, Koji / Shimoyama, Atsushi / Yoshii, Ken / Yamaura, Haruki / Nagatake, Takahiro / Nishino, Tomomi / Kiyono, Hiroshi / Fukase, Koichi / Kunisawa, Jun

    Vaccines

    2020  Volume 8, Issue 3

    Abstract: ... ...

    Abstract Alcaligenes
    Language English
    Publishing date 2020-07-20
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2703319-3
    ISSN 2076-393X
    ISSN 2076-393X
    DOI 10.3390/vaccines8030395
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Expression and role of the TGF-β family in glial cells infected with Borna disease virus.

    Nishino, Yoshii / Murakami, Masaru / Funaba, Masayuki

    Microbes and infection

    2016  Volume 18, Issue 2, Page(s) 128–136

    Abstract: A previous study revealed that the expression of the Borna disease virus (BDV)-encoding phosphoprotein in glial cells was sufficient to induce neurobehavioral abnormalities resembling Borna disease. To evaluate the involvement of the TGF-β family in BDV- ... ...

    Abstract A previous study revealed that the expression of the Borna disease virus (BDV)-encoding phosphoprotein in glial cells was sufficient to induce neurobehavioral abnormalities resembling Borna disease. To evaluate the involvement of the TGF-β family in BDV-induced changes in cell responses by C6 glial cells, we examined the expression levels of the TGF-β family and effects of inhibiting the TGF-β family pathway in BDV-infected C6 (C6BV) cells. The expression of activin βA and BMP7 was markedly increased in BDV-infected cells. Expression of Smad7, a TGF-β family-inducible gene, was increased by BDV infection, and the expression was decreased by treatment with A-83-01 or LDN-193189, inhibitors of the TGF-β/activin or BMP pathway, respectively. These results suggest autocrine effects of activin A and BMP7 in C6BV cells. IGFBP-3 expression was also induced by BDV infection; it was below the detection limit in C6 cells. The expression level of IGFBP-3 was decreased by LDN-193189 in C6BV cells, suggesting that endogenous BMP activity is responsible for IGFBP-3 gene induction. Our results reveal the regulatory expression of genes related to the TGF-β family, and the role of the enhanced BMP pathway in modulating cell responses in BDV-infected glial cells.
    MeSH term(s) Animals ; Borna disease virus/growth & development ; Cell Line ; Gene Expression Profiling ; Gene Regulatory Networks ; Host-Pathogen Interactions ; Neuroglia/virology ; Rats ; Transforming Growth Factor beta/antagonists & inhibitors ; Transforming Growth Factor beta/metabolism
    Chemical Substances Transforming Growth Factor beta
    Language English
    Publishing date 2016-02
    Publishing country France
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1465093-9
    ISSN 1769-714X ; 1286-4579
    ISSN (online) 1769-714X
    ISSN 1286-4579
    DOI 10.1016/j.micinf.2015.10.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Adjuvant Activity of Synthetic Lipid A of Alcaligenes , a Gut-Associated Lymphoid Tissue-Resident Commensal Bacterium, to Augment Antigen-Specific IgG and Th17 Responses in Systemic Vaccine

    Yunru Wang / Koji Hosomi / Atsushi Shimoyama / Ken Yoshii / Haruki Yamaura / Takahiro Nagatake / Tomomi Nishino / Hiroshi Kiyono / Koichi Fukase / Jun Kunisawa

    Vaccines, Vol 8, Iss 395, p

    2020  Volume 395

    Abstract: Alcaligenes spp. are identified as commensal bacteria and have been found to inhabit Peyer’s patches in the gut. We previously reported that Alcaligenes -derived lipopolysaccharides (LPS) exerted adjuvant activity in systemic vaccination, without ... ...

    Abstract Alcaligenes spp. are identified as commensal bacteria and have been found to inhabit Peyer’s patches in the gut. We previously reported that Alcaligenes -derived lipopolysaccharides (LPS) exerted adjuvant activity in systemic vaccination, without excessive inflammation. Lipid A is one of the components responsible for the biological effect of LPS and has previously been applied as an adjuvant. Here, we examined the adjuvant activity and safety of chemically synthesized Alcaligenes lipid A. We found that levels of OVA-specific serum IgG antibodies increased in mice that were subcutaneously immunized with ovalbumin (OVA) plus Alcaligenes lipid A relative to those that were immunized with OVA alone. In addition, Alcaligenes lipid A promoted antigen-specific T helper 17 (Th17) responses in the spleen; upregulated the expression of MHC class II, CD40, CD80, and CD86 on bone marrow-derived dendritic cells (BMDCs); enhanced the production of Th17-inducing cytokines IL-6 and IL-23 from BMDCs. Stimulation with Alcaligenes lipid A also induced the production of IL-6 and IL-1β in human peripheral blood mononuclear cells. Moreover, Alcaligenes lipid A caused minor side effects, such as lymphopenia and thrombocytopenia. These findings suggest that Alcaligenes lipid A is a safe and effective Th17-type adjuvant by directly stimulating dendritic cells in systemic vaccination.
    Keywords Alcaligenes faecalis ; Th17 ; lipid A ; Medicine ; R
    Language English
    Publishing date 2020-07-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Adaptive expression of uncoupling protein 1 in the carp liver and kidney in response to changes in ambient temperature.

    Murakami, Masaru / Ohi, Masahiro / Ishikawa, Shoko / Shirai, Mitsuyuki / Horiguchi, Hiroki / Nishino, Yoshii / Funaba, Masayuki

    Comparative biochemistry and physiology. Part A, Molecular & integrative physiology

    2015  Volume 185, Page(s) 142–149

    Abstract: The expression of uncoupling protein (UCP1) is up-regulated in mammalian brown adipocytes during cold exposure. However, a previous study revealed that UCP1 was highly expressed in the liver of common carps, and that the hepatic expression of UCP1 was ... ...

    Abstract The expression of uncoupling protein (UCP1) is up-regulated in mammalian brown adipocytes during cold exposure. However, a previous study revealed that UCP1 was highly expressed in the liver of common carps, and that the hepatic expression of UCP1 was down-regulated during cold exposure. The present study examined the effects of temperature on the recovery of UCP1 expression levels and the expression of genes involved in UCP1 transcription in the livers and kidneys of common carps. The hepatic and renal expressions of UCP1 were decreased by acclimation from 22 °C to 8 °C, and a subsequent increase in the water temperature from 8 °C to 28 °C recovered the renal, but not hepatic expression of UCP1. Changes in the expression of peroxisome proliferator-activator receptor (PPAR) γ, retinoid X receptor (RXR) α and PPARγ co-activator (PGC)-1α, genes that are involved in the expression of UCP1 in mammals, with ambient temperature indicated that the expressions of PPARγ and RXRα, but not expression of PGC-1α was decreased in response to cold exposure; the hepatic and renal expressions of PPARγ and RXRα recovered to basal levels with the cessation of cold exposure, although this was not complete for hepatic expression of PPARγ. The results of the present study indicate that a unique regulatory mechanism is responsible for the hepatic and renal expressions of carp UCP1 during cold exposure and subsequent reacclimation, and is distinct from that in murine brown adipocytes.
    MeSH term(s) Adaptation, Physiological ; Amino Acid Sequence ; Animals ; Base Sequence ; Carps/metabolism ; Fish Proteins/genetics ; Fish Proteins/metabolism ; Gene Expression Regulation ; Ion Channels/genetics ; Ion Channels/metabolism ; Kidney/metabolism ; Liver/metabolism ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Molecular Sequence Data ; Organ Specificity ; Temperature ; Uncoupling Protein 1
    Chemical Substances Fish Proteins ; Ion Channels ; Mitochondrial Proteins ; Uncoupling Protein 1
    Language English
    Publishing date 2015-07
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 121246-1
    ISSN 1531-4332 ; 0300-9629 ; 1095-6433
    ISSN (online) 1531-4332
    ISSN 0300-9629 ; 1095-6433
    DOI 10.1016/j.cbpa.2015.04.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Friction and Wear Properties of PTFE Sliding Seals -Influence of Surface Conditions of Seal Gland on Friction Properties-

    Chiharu Tadokoro / Yasuo Yoshii / Hitoshi Hattori / Daisuke Nishino

    Tribology Online, Vol 5, Iss 6, Pp 266-

    2010  Volume 270

    Abstract: Sealing devices are needed to prevent dust and water invading the positioning mechanisms of outdoor equipment. The frictional resistance generated by the seal frequently obstructs the smooth motion of the mechanism. The friction properties for high-speed ...

    Abstract Sealing devices are needed to prevent dust and water invading the positioning mechanisms of outdoor equipment. The frictional resistance generated by the seal frequently obstructs the smooth motion of the mechanism. The friction properties for high-speed and precision control mechanisms are required to be low and stable without lowering the sealing performance. In this study, the influence of the surface conditions of seal gland for PTFE sliding seal on friction properties was investigated experimentally. As a result, it has been found that the suitable surface condition of the seal gland for a high-speed and precision control mechanism is the electroless-nickel-plated surface of 0.1 μm Ra
    Keywords seal ; ptfe composite ; surface modification ; surface roughness ; friction ; Physics ; QC1-999 ; Engineering (General). Civil engineering (General) ; TA1-2040 ; Mechanical engineering and machinery ; TJ1-1570 ; Chemistry ; QD1-999
    Subject code 621
    Language English
    Publishing date 2010-11-01T00:00:00Z
    Publisher Japanese Society of Tribologists
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article: Adaptive expression of uncoupling protein 1 in the carp liver and kidney in response to changes in ambient temperature

    Murakami, Masaru / Hiroki Horiguchi / Masahiro Ohi / Masayuki Funaba / Mitsuyuki Shirai / Shoko Ishikawa / Yoshii Nishino

    Comparative biochemistry and physiology. 2015 July, v. 185

    2015  

    Abstract: The expression of uncoupling protein (UCP1) is up-regulated in mammalian brown adipocytes during cold exposure. However, a previous study revealed that UCP1 was highly expressed in the liver of common carps, and that the hepatic expression of UCP1 was ... ...

    Abstract The expression of uncoupling protein (UCP1) is up-regulated in mammalian brown adipocytes during cold exposure. However, a previous study revealed that UCP1 was highly expressed in the liver of common carps, and that the hepatic expression of UCP1 was down-regulated during cold exposure. The present study examined the effects of temperature on the recovery of UCP1 expression levels and the expression of genes involved in UCP1 transcription in the livers and kidneys of common carps. The hepatic and renal expressions of UCP1 were decreased by acclimation from 22°C to 8°C, and a subsequent increase in the water temperature from 8°C to 28°C recovered the renal, but not hepatic expression of UCP1. Changes in the expression of peroxisome proliferator-activator receptor (PPAR) γ, retinoid X receptor (RXR) α and PPARγ co-activator (PGC)-1α, genes that are involved in the expression of UCP1 in mammals, with ambient temperature indicated that the expressions of PPARγ and RXRα, but not expression of PGC-1α was decreased in response to cold exposure; the hepatic and renal expressions of PPARγ and RXRα recovered to basal levels with the cessation of cold exposure, although this was not complete for hepatic expression of PPARγ. The results of the present study indicate that a unique regulatory mechanism is responsible for the hepatic and renal expressions of carp UCP1 during cold exposure and subsequent reacclimation, and is distinct from that in murine brown adipocytes.
    Keywords acclimation ; adipocytes ; ambient temperature ; brown adipose tissue ; carp ; cold stress ; gene expression ; genes ; kidneys ; liver ; mice ; peroxisome proliferator-activated receptors ; water temperature
    Language English
    Dates of publication 2015-07
    Size p. 142-149.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 121246-1
    ISSN 1531-4332 ; 0300-9629 ; 1095-6433
    ISSN (online) 1531-4332
    ISSN 0300-9629 ; 1095-6433
    DOI 10.1016/j.cbpa.2015.04.003
    Database NAL-Catalogue (AGRICOLA)

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  7. Article ; Online: Regulatory expression of genes related to metastasis by TGF-beta and activin A in B16 murine melanoma cells.

    Murakami, Masaru / Suzuki, Makiko / Nishino, Yoshii / Funaba, Masayuki

    Molecular biology reports

    2009  Volume 37, Issue 3, Page(s) 1279–1286

    Abstract: TGF-beta induces epithelial-mesenchymal transition, which occurs during tumor cell invasiveness in pathological state, in limited cells. As a first step to understand the role of TGF-beta and the structurally related activin during melanoma metastasis, ... ...

    Abstract TGF-beta induces epithelial-mesenchymal transition, which occurs during tumor cell invasiveness in pathological state, in limited cells. As a first step to understand the role of TGF-beta and the structurally related activin during melanoma metastasis, expression of metastasis-related genes was examined in murine melanoma cells. Treatment with TGF-beta1 or activin A down-regulated E-cadherin in B16 cells in a dose-dependent manner. In epithelial cells, TGF-beta-induced high mobility group A2 (HMGA2) gene product is suggested to down-regulate E-cadherin through up-regulation of zinc-finger transcription factors Slug and Snail, and basic helix-loop-helix transcription factor Twist. Unlike the regulation in epithelial cells, TGF-beta1 treatment rather decreased mRNA expression of HMGA2, indicating a distinct mechanism on TGF-beta/activin-induced down-regulation. Transfection of double-stranded interfering RNA (dsRNAi) for activin receptor-like kinase (ALK) type I receptors revealed that ALK5, a prototype of TGF-beta receptor, mainly transmits TGF-beta signals on the E-cadherin down-regulation at the mRNA level, and that a prototype receptor ALK4 elicited the activin effect. TGF-beta/activin potentiated down-regulation of E-cadherin and HMGA2 also in B16 sublines that are susceptible to metastasis. However, the extent of down-regulation tended to be smaller, and less Smad2, a signal mediator for TGF-beta/activin, was phosphorylated in response to the ligand, resulting from less expression of type I receptors in the B16 sublines. These results suggest that the receptor expression level determines strength of the signals for TGF-beta/activin through phosphorylation of Smad2, which explains pluripotency of the ligand family partly.
    MeSH term(s) Activin Receptors, Type I/metabolism ; Activins/pharmacology ; Animals ; Blotting, Western ; Cadherins/metabolism ; Cell Line, Tumor ; DNA Primers/genetics ; Gene Expression Regulation, Neoplastic/drug effects ; Gene Expression Regulation, Neoplastic/genetics ; Melanoma, Experimental/metabolism ; Mice ; Oligonucleotides/genetics ; Phosphorylation ; Protein-Serine-Threonine Kinases/metabolism ; RNA Interference ; RNA, Double-Stranded/genetics ; Receptor, Transforming Growth Factor-beta Type I ; Receptors, Transforming Growth Factor beta/metabolism ; Smad2 Protein/metabolism ; Transforming Growth Factor beta/pharmacology
    Chemical Substances Cadherins ; DNA Primers ; Oligonucleotides ; RNA, Double-Stranded ; Receptors, Transforming Growth Factor beta ; Smad2 Protein ; Smad2 protein, mouse ; Transforming Growth Factor beta ; activin A ; Activins (104625-48-1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Activin Receptors, Type I (EC 2.7.11.30) ; Acvr1b protein, mouse (EC 2.7.11.30) ; Receptor, Transforming Growth Factor-beta Type I (EC 2.7.11.30) ; Tgfbr1 protein, mouse (EC 2.7.11.30)
    Language English
    Publishing date 2009-03-14
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 186544-4
    ISSN 1573-4978 ; 0301-4851
    ISSN (online) 1573-4978
    ISSN 0301-4851
    DOI 10.1007/s11033-009-9502-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Nucleotide sequence of canine Smad3.

    Sugiyama, Kazutoshi / Ooishi, Ryo / Nishino, Yoshii / Funaba, Masayuki / Murakami, Masaru

    Biochemical genetics

    2010  Volume 48, Issue 3-4, Page(s) 202–207

    Abstract: The whole genome sequence of a Boxer dog suggested that the amino acid sequence of the carboxyl terminus of a putative Smad3 is SSVF-(COOH), not SSVS-(COOH) as in all Smad3 sequences identified in many species. Because phosphorylation of the last two ... ...

    Abstract The whole genome sequence of a Boxer dog suggested that the amino acid sequence of the carboxyl terminus of a putative Smad3 is SSVF-(COOH), not SSVS-(COOH) as in all Smad3 sequences identified in many species. Because phosphorylation of the last two serines at the carboxyl terminus is generally indispensable for Smad3-mediated signaling, the role of Smad3 may be unique in dogs. The present study determines the nucleotide sequence of the coding region of canine Smad3 and deduces the carboxyl terminal amino acids of Smad3 in several breeds. Except for the Boxer, the deduced amino acid sequence was SSVS-(COOH) in all dogs examined. In addition, the nucleotide at position 1204 in the Boxer was different from that of the other dogs. Furthermore, there was a SNP at nt 240. The present study indicates that the carboxyl terminal amino acid of canine Smad3 is not unique, although it is unknown in the Boxer breed.
    MeSH term(s) Amino Acid Sequence ; Animals ; Base Sequence ; Breeding ; Cloning, Molecular ; Dogs/genetics ; Genetic Variation/physiology ; Molecular Sequence Data ; Protein Structure, Tertiary/genetics ; Sequence Analysis, DNA ; Smad3 Protein/chemistry ; Smad3 Protein/genetics ; Species Specificity
    Chemical Substances Smad3 Protein
    Language English
    Publishing date 2010-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2168-4
    ISSN 1573-4927 ; 0006-2928
    ISSN (online) 1573-4927
    ISSN 0006-2928
    DOI 10.1007/s10528-009-9304-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Changes in Borna disease virus genome with adaptation to host.

    Okayama, Satoshi / Miura, Nanako / Murakami, Masaru / Funaba, Masayuki / Nishino, Yoshii

    Microbes and infection

    2009  Volume 11, Issue 6-7, Page(s) 721–724

    Abstract: The CRNP5 variant of Borna disease virus (BDV) has stronger pathogenesis than the CRP3 variant in which only 4 nucleotides in the whole genome are different. The CRP3 is produced by 3 passages in rat brains of BDV, whereas the CRNP5 is produced by 5 ... ...

    Abstract The CRNP5 variant of Borna disease virus (BDV) has stronger pathogenesis than the CRP3 variant in which only 4 nucleotides in the whole genome are different. The CRP3 is produced by 3 passages in rat brains of BDV, whereas the CRNP5 is produced by 5 passages in mouse brains after 2 passages in rat brains of the BDV. Thymidylic acids at nt 3608 and 3673 were replaced by cytidylic acids during 3 passages in mice. Three passages in mice caused replacement of adenylic acid at nt 7936 by guanylic acid. No replacement at nt 8742 occurred during passages in mice.
    MeSH term(s) Adaptation, Biological ; Animals ; Animals, Newborn ; Borna disease virus/genetics ; Borna disease virus/growth & development ; Brain/virology ; Genome, Viral ; Mice ; Point Mutation ; Rats ; Serial Passage
    Language English
    Publishing date 2009-05
    Publishing country France
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1465093-9
    ISSN 1769-714X ; 1286-4579
    ISSN (online) 1769-714X
    ISSN 1286-4579
    DOI 10.1016/j.micinf.2009.03.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Regulatory expression of genes related to metastasis by TGF-β and activin A in B16 murine melanoma cells

    Murakami, Masaru / Suzuki, Makiko / Nishino, Yoshii / Funaba, Masayuki

    Molecular biology reports. 2010 Mar., v. 37, no. 3

    2010  

    Abstract: TGF-β induces epithelial-mesenchymal transition, which occurs during tumor cell invasiveness in pathological state, in limited cells. As a first step to understand the role of TGF-β and the structurally related activin during melanoma metastasis, ... ...

    Abstract TGF-β induces epithelial-mesenchymal transition, which occurs during tumor cell invasiveness in pathological state, in limited cells. As a first step to understand the role of TGF-β and the structurally related activin during melanoma metastasis, expression of metastasis-related genes was examined in murine melanoma cells. Treatment with TGF-β1 or activin A down-regulated E-cadherin in B16 cells in a dose-dependent manner. In epithelial cells, TGF-β-induced high mobility group A2 (HMGA2) gene product is suggested to down-regulate E-cadherin through up-regulation of zinc-finger transcription factors Slug and Snail, and basic helix-loop-helix transcription factor Twist. Unlike the regulation in epithelial cells, TGF-β1 treatment rather decreased mRNA expression of HMGA2, indicating a distinct mechanism on TGF-β/activin-induced down-regulation. Transfection of double-stranded interfering RNA (dsRNAi) for activin receptor-like kinase (ALK) type I receptors revealed that ALK5, a prototype of TGF-β receptor, mainly transmits TGF-β signals on the E-cadherin down-regulation at the mRNA level, and that a prototype receptor ALK4 elicited the activin effect. TGF-β/activin potentiated down-regulation of E-cadherin and HMGA2 also in B16 sublines that are susceptible to metastasis. However, the extent of down-regulation tended to be smaller, and less Smad2, a signal mediator for TGF-β/activin, was phosphorylated in response to the ligand, resulting from less expression of type I receptors in the B16 sublines. These results suggest that the receptor expression level determines strength of the signals for TGF-β/activin through phosphorylation of Smad2, which explains pluripotency of the ligand family partly.
    Keywords basic helix-loop-helix transcription factors ; epithelial cells ; gene expression ; gene expression regulation ; genes ; melanoma ; messenger RNA ; metastasis ; mice ; receptors ; transfection ; transforming growth factor beta 1
    Language English
    Dates of publication 2010-03
    Size p. 1279-1286.
    Publisher Springer Netherlands
    Publishing place Dordrecht
    Document type Article
    ZDB-ID 186544-4
    ISSN 1573-4978 ; 0301-4851
    ISSN (online) 1573-4978
    ISSN 0301-4851
    DOI 10.1007/s11033-009-9502-x
    Database NAL-Catalogue (AGRICOLA)

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