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  1. Book ; Online: New Trends in Vascular Inflammation Research: From Biology to Therapy

    Aikawa, Masanori / Manabe, Ichiro / Marx, Nikolaus

    2019  

    Keywords Medicine ; Inflammation ; Atherosclerosis ; cardiometabolic disease ; monocyte ; macrophage ; therapy ; Aging ; senescence ; Efferocytosis ; regression
    Size 1 electronic resource (193 pages)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT021230225
    ISBN 9782889456376 ; 2889456374
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Article: Inflammaging and age-associated diseases.

    Manabe, Ichiro

    Nihon Ronen Igakkai zasshi. Japanese journal of geriatrics

    2017  Volume 54, Issue 2, Page(s) 105–113

    MeSH term(s) Aged ; Aging/physiology ; Humans ; Inflammation/pathology
    Language Japanese
    Publishing date 2017-06-12
    Publishing country Japan
    Document type Journal Article ; Review
    ZDB-ID 604107-3
    ISSN 0300-9173
    ISSN 0300-9173
    DOI 10.3143/geriatrics.54.105
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1039: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  3. Article ; Online: Nerve-macrophage interactions in cardiovascular disease.

    Fujiu, Katsuhito / Manabe, Ichiro

    International immunology

    2021  Volume 34, Issue 2, Page(s) 81–95

    Abstract: The heart is highly innervated by autonomic neurons, and dynamic autonomic regulation of the heart and blood vessels is essential for animals to carry out the normal activities of life. Cardiovascular diseases, including heart failure and myocardial ... ...

    Abstract The heart is highly innervated by autonomic neurons, and dynamic autonomic regulation of the heart and blood vessels is essential for animals to carry out the normal activities of life. Cardiovascular diseases, including heart failure and myocardial infarction, are characterized in part by an imbalance in autonomic nervous system activation, with excess sympathetic and diminished parasympathetic activation. Notably, however, this is often accompanied by chronic inflammation within the cardiovascular tissues, which suggests there are interactions between autonomic dysregulation and inflammation. Recent studies have been unraveling the mechanistic links between autonomic nerves and immune cells within the cardiovascular system. The autonomic nervous system and immune system also act in concert to coordinate the actions of multiple organs that not only maintain homeostasis but also likely play key roles in disease-disease interactions, such as cardiorenal syndrome and multimorbidity. In this review, we summarize the physiological and pathological interactions between autonomic nerves and macrophages in the context of cardiovascular disease.
    MeSH term(s) Animals ; Autonomic Nervous System/physiology ; Cardiovascular Diseases ; Heart/innervation ; Inflammation ; Macrophages
    Language English
    Publishing date 2021-06-26
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1013745-2
    ISSN 1460-2377 ; 0953-8178
    ISSN (online) 1460-2377
    ISSN 0953-8178
    DOI 10.1093/intimm/dxab036
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2619: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)
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  4. Article ; Online: Caspase-11 contributes to site-1 protease cleavage and SREBP1 activation in the inflammatory response of macrophages.

    Cheng, Yinglan / Manabe, Ichiro / Hayakawa, Sumio / Endo, Yusuke / Oishi, Yumiko

    Frontiers in immunology

    2023  Volume 14, Page(s) 1009973

    Abstract: Sterol regulatory element-binding proteins (SREBPs) are key transcription factors that control fatty acid and cholesterol metabolism. As the major SREBP isoform in macrophages, SREBP1a is also required for inflammatory and phagocytotic functions. However, ...

    Abstract Sterol regulatory element-binding proteins (SREBPs) are key transcription factors that control fatty acid and cholesterol metabolism. As the major SREBP isoform in macrophages, SREBP1a is also required for inflammatory and phagocytotic functions. However, it is insufficiently understood how SREBP1a is activated by the innate immune response in macrophages. Here, we show that mouse caspase-11 is a novel inflammatory activator of SREBP1a in macrophages. Upon LPS treatment, caspase-11 was found to promote the processing of site-1 protease (S1P), an enzyme that mediates the cleavage and activation of SREBP1. We also determined that caspase-11 directly associates with S1P and cleaves it at a specific site. Furthermore, deletion of the
    MeSH term(s) Animals ; Mice ; Caspases ; Lipopolysaccharides ; Macrophages/metabolism ; Sterol Regulatory Element Binding Protein 1/genetics ; Sterol Regulatory Element Binding Protein 1/metabolism
    Chemical Substances Caspases (EC 3.4.22.-) ; Lipopolysaccharides ; membrane-bound transcription factor peptidase, site 1 (EC 3.4.21.112) ; Sterol Regulatory Element Binding Protein 1
    Language English
    Publishing date 2023-01-27
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1009973
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Mechanisms of cooperative cell-cell interactions in skeletal muscle regeneration.

    Koike, Hiroyuki / Manabe, Ichiro / Oishi, Yumiko

    Inflammation and regeneration

    2022  Volume 42, Issue 1, Page(s) 48

    Abstract: Skeletal muscles have an extraordinary capacity to regenerate themselves when injured. Skeletal muscle stem cells, called satellite cells, play a central role in muscle regeneration via three major steps: activation, proliferation, and differentiation. ... ...

    Abstract Skeletal muscles have an extraordinary capacity to regenerate themselves when injured. Skeletal muscle stem cells, called satellite cells, play a central role in muscle regeneration via three major steps: activation, proliferation, and differentiation. These steps are affected by multiple types of cells, such as immune cells, fibro-adipogenic progenitor cells, and vascular endothelial cells. The widespread use of single-cell sequencing technologies has enabled the identification of novel cell subpopulations associated with muscle regeneration and their regulatory mechanisms. This review summarizes the dynamism of the cellular community that controls and promotes muscle regeneration, with a particular focus on skeletal muscle stem cells.
    Language English
    Publishing date 2022-11-16
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2051471-2
    ISSN 1880-9693 ; 0389-4290
    ISSN 1880-9693 ; 0389-4290
    DOI 10.1186/s41232-022-00234-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.B 2929: Show issues Location:
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  6. Article ; Online: VDR regulates simulated microgravity-induced atrophy in C2C12 myotubes.

    Yuzawa, Ryo / Koike, Hiroyuki / Manabe, Ichiro / Oishi, Yumiko

    Scientific reports

    2022  Volume 12, Issue 1, Page(s) 1377

    Abstract: Muscle wasting is a major problem leading to reduced quality of life and higher risks of mortality and various diseases. Muscle atrophy is caused by multiple conditions in which protein degradation exceeds its synthesis, including disuse, malnutrition, ... ...

    Abstract Muscle wasting is a major problem leading to reduced quality of life and higher risks of mortality and various diseases. Muscle atrophy is caused by multiple conditions in which protein degradation exceeds its synthesis, including disuse, malnutrition, and microgravity. While Vitamin D receptor (VDR) is well known to regulate calcium and phosphate metabolism to maintain bone, recent studies have shown that VDR also plays roles in skeletal muscle development and homeostasis. Moreover, its expression is upregulated in muscle undergoing atrophy as well as after muscle injury. Here we show that VDR regulates simulated microgravity-induced atrophy in C2C12 myotubes in vitro. After 8 h of microgravity simulated using 3D-clinorotation, the VDR-binding motif was associated with chromatin regions closed by the simulated microgravity and enhancer regions inactivated by it, which suggests VDR mediates repression of enhancers. In addition, VDR was induced and translocated into the nuclei in response to simulated microgravity. VDR-deficient C2C12 myotubes showed resistance to simulated microgravity-induced atrophy and reduced induction of FBXO32, an atrophy-associated ubiquitin ligase. These results demonstrate that VDR contributes to the regulation of simulated microgravity-induced atrophy at least in part by controlling expression of atrophy-related genes.
    MeSH term(s) Animals ; Cell Line ; Gene Knockout Techniques/methods ; Homeostasis/genetics ; Mice ; Muscle Development/genetics ; Muscle Fibers, Skeletal/metabolism ; Muscular Atrophy/etiology ; Muscular Atrophy/genetics ; Muscular Atrophy/metabolism ; Myoblasts, Skeletal/metabolism ; Receptors, Calcitriol/genetics ; Receptors, Calcitriol/metabolism ; Signal Transduction/genetics ; Transfection ; Weightlessness Simulation/adverse effects
    Chemical Substances Receptors, Calcitriol ; Vdr protein, mouse
    Language English
    Publishing date 2022-01-26
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-022-05354-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Organ System Crosstalk in Cardiometabolic Disease in the Age of Multimorbidity.

    Oishi, Yumiko / Manabe, Ichiro

    Frontiers in cardiovascular medicine

    2020  Volume 7, Page(s) 64

    Abstract: The close association among cardiovascular, metabolic, and kidney diseases suggests a common pathological basis and significant interaction among these diseases. Metabolic syndrome and cardiorenal syndrome are two examples that exemplify the interlinked ... ...

    Abstract The close association among cardiovascular, metabolic, and kidney diseases suggests a common pathological basis and significant interaction among these diseases. Metabolic syndrome and cardiorenal syndrome are two examples that exemplify the interlinked development of disease or dysfunction in two or more organs. Recent studies have been sorting out the mechanisms responsible for the crosstalk among the organs comprising the cardiovascular, metabolic, and renal systems, including heart-kidney and adipose-liver signaling, among many others. However, it is also becoming clear that this crosstalk is not limited to just pairs of organs, and in addition to organ-organ crosstalk, there are also organ-system and organ-body interactions. For instance, heart failure broadly impacts various organs and systems, including the kidney, liver, lung, and nervous system. Conversely, systemic dysregulation of metabolism, immunity, and nervous system activity greatly affects heart failure development and prognosis. This is particularly noteworthy, as more and more patients present with two or more coexisting chronic diseases or conditions (multimorbidity) due in part to the aging of society. Advances in treatment also contribute to the increase in multimorbidity, as exemplified by cardiovascular disease in cancer survivors. To understand the mechanisms underlying the increasing burden of multimorbidity, it is vital to elucidate the multilevel crosstalk and communication within the body at the levels of organ systems, tissues, and cells. In this article, we focus on chronic inflammation as a key common pathological basis of cardiovascular and metabolic diseases, and discuss emerging mechanisms that drive chronic inflammation in the context of multimorbidity.
    Language English
    Publishing date 2020-04-28
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2781496-8
    ISSN 2297-055X
    ISSN 2297-055X
    DOI 10.3389/fcvm.2020.00064
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: VDR regulates simulated microgravity-induced atrophy in C2C12 myotubes

    Ryo Yuzawa / Hiroyuki Koike / Ichiro Manabe / Yumiko Oishi

    Scientific Reports, Vol 12, Iss 1, Pp 1-

    2022  Volume 11

    Abstract: Abstract Muscle wasting is a major problem leading to reduced quality of life and higher risks of mortality and various diseases. Muscle atrophy is caused by multiple conditions in which protein degradation exceeds its synthesis, including disuse, ... ...

    Abstract Abstract Muscle wasting is a major problem leading to reduced quality of life and higher risks of mortality and various diseases. Muscle atrophy is caused by multiple conditions in which protein degradation exceeds its synthesis, including disuse, malnutrition, and microgravity. While Vitamin D receptor (VDR) is well known to regulate calcium and phosphate metabolism to maintain bone, recent studies have shown that VDR also plays roles in skeletal muscle development and homeostasis. Moreover, its expression is upregulated in muscle undergoing atrophy as well as after muscle injury. Here we show that VDR regulates simulated microgravity-induced atrophy in C2C12 myotubes in vitro. After 8 h of microgravity simulated using 3D-clinorotation, the VDR-binding motif was associated with chromatin regions closed by the simulated microgravity and enhancer regions inactivated by it, which suggests VDR mediates repression of enhancers. In addition, VDR was induced and translocated into the nuclei in response to simulated microgravity. VDR-deficient C2C12 myotubes showed resistance to simulated microgravity-induced atrophy and reduced induction of FBXO32, an atrophy-associated ubiquitin ligase. These results demonstrate that VDR contributes to the regulation of simulated microgravity-induced atrophy at least in part by controlling expression of atrophy-related genes.
    Keywords Medicine ; R ; Science ; Q
    Subject code 616
    Language English
    Publishing date 2022-01-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Arntl deficiency in myeloid cells reduces neutrophil recruitment and delays skeletal muscle repair.

    Watanabe, Aiko / Koike, Hiroyuki / Kumagami, Naoki / Shimba, Shigeki / Manabe, Ichiro / Oishi, Yumiko

    Scientific reports

    2023  Volume 13, Issue 1, Page(s) 6747

    Abstract: After a muscle injury, a process comprising inflammation, repair, and regeneration must occur in a time-sensitive manner for skeletal muscle to be adequately repaired and regenerated. This complex process is assumed to be controlled by various myeloid ... ...

    Abstract After a muscle injury, a process comprising inflammation, repair, and regeneration must occur in a time-sensitive manner for skeletal muscle to be adequately repaired and regenerated. This complex process is assumed to be controlled by various myeloid cell types, including monocytes and macrophages, though the mechanism is not fully understood. Aryl hydrocarbon receptor nuclear translocator-like (Arntl or Bmal1) is a transcription factor that controls the circadian rhythm and has been implicated in regulating myeloid cell functions. In the present study, we generated myeloid cell-specific Arntl conditional knockout (cKO) mice to assess the role of Arntl expressed in myeloid cell populations during the repair process after muscle injury. Myeloid cell-specific Arntl deletion impaired muscle regeneration after cardiotoxin injection. Flow cytometric analyses revealed that, in cKO mice, the numbers of infiltrating neutrophils and Ly6C
    MeSH term(s) Animals ; Mice ; ARNTL Transcription Factors/metabolism ; Macrophages/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Monocytes/metabolism ; Muscle, Skeletal/metabolism ; Muscular Diseases/metabolism ; Myeloid Cells/metabolism ; Neutrophil Infiltration ; Regeneration/physiology
    Chemical Substances ARNTL Transcription Factors
    Language English
    Publishing date 2023-04-25
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-023-33830-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Characteristic impairment of progesterone response in cultured cervical fibroblasts obtained from patients with refractory cervical insufficiency.

    Sugita, Yosuke / Kuwabara, Yoshimitsu / Katayama, Akira / Matsuda, Shigeru / Manabe, Ichiro / Suzuki, Shunji / Oishi, Yumiko

    Scientific reports

    2023  Volume 13, Issue 1, Page(s) 11709

    Abstract: Preterm birth (PTB) is the leading cause of neonatal mortality, and reducing the PTB rate is one of the most critical issues in perinatal medicine. Cervical insufficiency (CI), a major cause of PTB, is characterised by premature cervical ripening in the ... ...

    Abstract Preterm birth (PTB) is the leading cause of neonatal mortality, and reducing the PTB rate is one of the most critical issues in perinatal medicine. Cervical insufficiency (CI), a major cause of PTB, is characterised by premature cervical ripening in the second trimester, followed by recurrent pregnancy loss. Although multiple clinical trials have suggested that progesterone inhibits cervical ripening, no studies have focused on progesterone-induced molecular signalling in CI. Here, we established a primary culture system for human uterine cervical fibroblasts using a sample of patients with refractory innate CI who underwent transabdominal cervical cerclage and patients with low Bishop scores who underwent elective caesarean section as controls. RNA sequencing showed that the progesterone response observed in the control group was impaired in the CI group. This was consistent with the finding that progesterone receptor expression was markedly downregulated in CI. Furthermore, the inhibitory effect of progesterone on lipopolysaccharide-induced inflammatory stimuli was also impaired in CI. These results suggest that abnormal cervical ripening in CI is caused by the downregulation of progesterone signalling at the receptor level, and provide a novel insight into the molecular mechanism of PTB.
    MeSH term(s) Humans ; Pregnancy ; Infant, Newborn ; Female ; Progesterone/pharmacology ; Progesterone/therapeutic use ; Premature Birth/drug therapy ; Cesarean Section ; Cerclage, Cervical/methods ; Cervix Uteri
    Chemical Substances Progesterone (4G7DS2Q64Y)
    Language English
    Publishing date 2023-07-20
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-023-37732-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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