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  1. Article ; Online: Multi-Omics of Familial Thoracic Aortic Aneurysm and Dissection: Calcium Transport Impairment Predisposes Aortas to Dissection.

    Tomida, Shota / Ishima, Tamaki / Sawaki, Daigo / Imai, Yasushi / Nagai, Ryozo / Aizawa, Kenichi

    International journal of molecular sciences

    2023  Volume 24, Issue 20

    Abstract: Several genetic defects, including a mutation in myosin heavy chain 11 ( ...

    Abstract Several genetic defects, including a mutation in myosin heavy chain 11 (
    MeSH term(s) Mice ; Animals ; Calcium/metabolism ; Multiomics ; Aorta/metabolism ; Aortic Aneurysm, Thoracic/metabolism ; Aorta, Thoracic/pathology
    Chemical Substances Calcium (SY7Q814VUP)
    Language English
    Publishing date 2023-10-16
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms242015213
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  2. Article ; Online: Weight loss to rejuvenate the heart.

    Derumeaux, Geneviève / Ernande, Laura / Sawaki, Daigo

    European heart journal cardiovascular Imaging

    2018  Volume 19, Issue 2, Page(s) 143–144

    MeSH term(s) Heart ; Humans ; Reoperation ; Weight Loss
    Language English
    Publishing date 2018--01
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 2638345-7
    ISSN 2047-2412 ; 2047-2404
    ISSN (online) 2047-2412
    ISSN 2047-2404
    DOI 10.1093/ehjci/jex318
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  3. Article ; Online: Response by Sawaki et al to Letter Regarding Article, "Visceral Adipose Tissue Drives Cardiac Aging Through Modulation of Fibroblast Senescence by Osteopontin Production".

    Sawaki, Daigo / Czibik, Gabor / Pini, Maria / Mezdari, Zaineb / Zhang, Yanyan / Henegar, Corneliu / Derumeaux, Geneviève

    Circulation

    2019  Volume 139, Issue 6, Page(s) 845–846

    MeSH term(s) Cellular Senescence ; Fibroblasts ; Heart ; Intra-Abdominal Fat ; Osteopontin
    Chemical Substances Osteopontin (106441-73-0)
    Language English
    Publishing date 2019-02-04
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.118.038482
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  4. Article ; Online: Targeting transforming growth factor-β signaling in aortopathies in Marfan syndrome.

    Sawaki, Daigo / Suzuki, Toru

    Circulation journal : official journal of the Japanese Circulation Society

    2013  Volume 77, Issue 4, Page(s) 898–899

    MeSH term(s) Aorta/metabolism ; Aortic Aneurysm/blood ; Female ; Humans ; Male ; Marfan Syndrome/blood ; Transforming Growth Factor beta1/biosynthesis
    Chemical Substances Transforming Growth Factor beta1
    Language English
    Publishing date 2013-02-14
    Publishing country Japan
    Document type Journal Article ; Comment
    ZDB-ID 2068090-9
    ISSN 1347-4820 ; 1346-9843
    ISSN (online) 1347-4820
    ISSN 1346-9843
    DOI 10.1253/circj.cj-13-0183
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  5. Article ; Online: Osteopontin promotes age-related adipose tissue remodeling through senescence-associated macrophage dysfunction.

    Sawaki, Daigo / Zhang, Yanyan / Mohamadi, Amel / Pini, Maria / Mezdari, Zaineb / Lipskaia, Larissa / Naushad, Suzain / Lamendour, Lucille / Altintas, Dogus Murat / Breau, Marielle / Liang, Hao / Halfaoui, Maissa / Delmont, Thaïs / Surenaud, Mathieu / Rousseau, Déborah / Yoshimitsu, Takehiko / Louache, Fawzia / Adnot, Serge / Henegar, Corneliu /
    Gual, Philippe / Czibik, Gabor / Derumeaux, Geneviève

    JCI insight

    2023  Volume 8, Issue 8

    Abstract: Adipose tissue macrophages (ATMs) play an important role in obesity and inflammation, and they accumulate in adipose tissue (AT) with aging. Furthermore, increased ATM senescence has been shown in obesity-related AT remodeling and dysfunction. However, ... ...

    Abstract Adipose tissue macrophages (ATMs) play an important role in obesity and inflammation, and they accumulate in adipose tissue (AT) with aging. Furthermore, increased ATM senescence has been shown in obesity-related AT remodeling and dysfunction. However, ATM senescence and its role are unclear in age-related AT dysfunction. Here, we show that ATMs (a) acquire a senescence-like phenotype during chronological aging; (b) display a global decline of basic macrophage functions such as efferocytosis, an essential process to preserve AT homeostasis by clearing dysfunctional or apoptotic cells; and (c) promote AT remodeling and dysfunction. Importantly, we uncover a major role for the age-associated accumulation of osteopontin (OPN) in these processes in visceral AT. Consistently, loss or pharmacologic inhibition of OPN and bone marrow transplantation of OPN-/- mice attenuate the ATM senescence-like phenotype, preserve efferocytosis, and finally restore healthy AT homeostasis in the context of aging. Collectively, our findings implicate pharmacologic OPN inhibition as a viable treatment modality to counter ATM senescence-mediated AT remodeling and dysfunction during aging.
    MeSH term(s) Mice ; Animals ; Osteopontin/genetics ; Obesity/genetics ; Adipose Tissue ; Macrophages ; Phagocytosis
    Chemical Substances Osteopontin (106441-73-0)
    Language English
    Publishing date 2023-04-24
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.145811
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  6. Article ; Online: Secretory GFP reconstitution labeling of neighboring cells interrogates cell-cell interactions in metastatic niches.

    Minegishi, Misa / Kuchimaru, Takahiro / Nishikawa, Kaori / Isagawa, Takayuki / Iwano, Satoshi / Iida, Kei / Hara, Hiromasa / Miura, Shizuka / Sato, Marika / Watanabe, Shigeaki / Shiomi, Akifumi / Mabuchi, Yo / Hamana, Hiroshi / Kishi, Hiroyuki / Sato, Tatsuyuki / Sawaki, Daigo / Sato, Shigeru / Hanazono, Yutaka / Suzuki, Atsushi /
    Kohro, Takahide / Kadonosono, Tetsuya / Shimogori, Tomomi / Miyawaki, Atsushi / Takeda, Norihiko / Shintaku, Hirofumi / Kizaka-Kondoh, Shinae / Nishimura, Satoshi

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 8031

    Abstract: Cancer cells inevitably interact with neighboring host tissue-resident cells during the process of metastatic colonization, establishing a metastatic niche to fuel their survival, growth, and invasion. However, the underlying mechanisms in the metastatic ...

    Abstract Cancer cells inevitably interact with neighboring host tissue-resident cells during the process of metastatic colonization, establishing a metastatic niche to fuel their survival, growth, and invasion. However, the underlying mechanisms in the metastatic niche are yet to be fully elucidated owing to the lack of methodologies for comprehensively studying the mechanisms of cell-cell interactions in the niche. Here, we improve a split green fluorescent protein (GFP)-based genetically encoded system to develop secretory glycosylphosphatidylinositol-anchored reconstitution-activated proteins to highlight intercellular connections (sGRAPHIC) for efficient fluorescent labeling of tissue-resident cells that neighbor on and putatively interact with cancer cells in deep tissues. The sGRAPHIC system enables the isolation of metastatic niche-associated tissue-resident cells for their characterization using a single-cell RNA sequencing platform. We use this sGRAPHIC-leveraged transcriptomic platform to uncover gene expression patterns in metastatic niche-associated hepatocytes in a murine model of liver metastasis. Among the marker genes of metastatic niche-associated hepatocytes, we identify Lgals3, encoding galectin-3, as a potential pro-metastatic factor that accelerates metastatic growth and invasion.
    MeSH term(s) Humans ; Mice ; Animals ; Liver Neoplasms/metabolism ; Hepatocytes/metabolism ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Extracellular Matrix/metabolism ; Cell Communication
    Chemical Substances Green Fluorescent Proteins (147336-22-9)
    Language English
    Publishing date 2023-12-05
    Publishing country England
    Document type Journal Article
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-43855-2
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  7. Article ; Online: Adipose tissue senescence is mediated by increased ATP content after a short-term high-fat diet exposure.

    Pini, Maria / Czibik, Gabor / Sawaki, Daigo / Mezdari, Zaineb / Braud, Laura / Delmont, Thaïs / Mercedes, Raquel / Martel, Cécile / Buron, Nelly / Marcelin, Geneviève / Borgne-Sanchez, Annie / Foresti, Roberta / Motterlini, Roberto / Henegar, Corneliu / Derumeaux, Geneviève

    Aging cell

    2021  Volume 20, Issue 8, Page(s) e13421

    Abstract: In the context of obesity, senescent cells accumulate in white adipose tissue (WAT). The cellular underpinnings of WAT senescence leading to insulin resistance are not fully elucidated. The objective of the current study was to evaluate the presence of ... ...

    Abstract In the context of obesity, senescent cells accumulate in white adipose tissue (WAT). The cellular underpinnings of WAT senescence leading to insulin resistance are not fully elucidated. The objective of the current study was to evaluate the presence of WAT senescence early after initiation of high-fat diet (HFD, 1-10 weeks) in 5-month-old male C57BL/6J mice and the potential role of energy metabolism. We first showed that WAT senescence occurred 2 weeks after HFD as evidenced in whole WAT by increased senescence-associated ß-galactosidase activity and cyclin-dependent kinase inhibitor 1A and 2A expression. WAT senescence affected various WAT cell populations, including preadipocytes, adipose tissue progenitors, and immune cells, together with adipocytes. WAT senescence was associated with higher glycolytic and mitochondrial activity leading to enhanced ATP content in HFD-derived preadipocytes, as compared with chow diet-derived preadipocytes. One-month daily exercise, introduced 5 weeks after HFD, was an effective senostatic strategy, since it reversed WAT cellular senescence, while reducing glycolysis and production of ATP. Interestingly, the beneficial effect of exercise was independent of body weight and fat mass loss. We demonstrated that WAT cellular senescence is one of the earliest events occurring after HFD initiation and is intimately linked to the metabolic state of the cells. Our data uncover a critical role for HFD-induced elevated ATP as a local danger signal inducing WAT senescence. Exercise exerts beneficial effects on adipose tissue bioenergetics in obesity, reversing cellular senescence, and metabolic abnormalities.
    MeSH term(s) Adenosine Triphosphate/metabolism ; Adipose Tissue/physiopathology ; Animals ; Diet, High-Fat/adverse effects ; Energy Metabolism/physiology ; Male ; Mice
    Chemical Substances Adenosine Triphosphate (8L70Q75FXE)
    Language English
    Publishing date 2021-07-18
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2113083-8
    ISSN 1474-9726 ; 1474-9718
    ISSN (online) 1474-9726
    ISSN 1474-9718
    DOI 10.1111/acel.13421
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  8. Article ; Online: Osteopontin promotes age-related adipose tissue remodeling through senescence-associated macrophage dysfunction

    Daigo Sawaki / Yanyan Zhang / Amel Mohamadi / Maria Pini / Zaineb Mezdari / Larissa Lipskaia / Suzain Naushad / Lucille Lamendour / Dogus Murat Altintas / Marielle Breau / Hao Liang / Maissa Halfaoui / Thaïs Delmont / Mathieu Surenaud / Déborah Rousseau / Takehiko Yoshimitsu / Fawzia Louache / Serge Adnot / Corneliu Henegar /
    Philippe Gual / Gabor Czibik / Geneviève Derumeaux

    JCI Insight, Vol 8, Iss

    2023  Volume 8

    Abstract: Adipose tissue macrophages (ATMs) play an important role in obesity and inflammation, and they accumulate in adipose tissue (AT) with aging. Furthermore, increased ATM senescence has been shown in obesity-related AT remodeling and dysfunction. However, ... ...

    Abstract Adipose tissue macrophages (ATMs) play an important role in obesity and inflammation, and they accumulate in adipose tissue (AT) with aging. Furthermore, increased ATM senescence has been shown in obesity-related AT remodeling and dysfunction. However, ATM senescence and its role are unclear in age-related AT dysfunction. Here, we show that ATMs (a) acquire a senescence-like phenotype during chronological aging; (b) display a global decline of basic macrophage functions such as efferocytosis, an essential process to preserve AT homeostasis by clearing dysfunctional or apoptotic cells; and (c) promote AT remodeling and dysfunction. Importantly, we uncover a major role for the age-associated accumulation of osteopontin (OPN) in these processes in visceral AT. Consistently, loss or pharmacologic inhibition of OPN and bone marrow transplantation of OPN–/– mice attenuate the ATM senescence-like phenotype, preserve efferocytosis, and finally restore healthy AT homeostasis in the context of aging. Collectively, our findings implicate pharmacologic OPN inhibition as a viable treatment modality to counter ATM senescence-mediated AT remodeling and dysfunction during aging.
    Keywords Aging ; Immunology ; Medicine ; R
    Subject code 616
    Language English
    Publishing date 2023-04-01T00:00:00Z
    Publisher American Society for Clinical investigation
    Document type Article ; Online
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  9. Article ; Online: Secretory GFP reconstitution labeling of neighboring cells interrogates cell–cell interactions in metastatic niches

    Misa Minegishi / Takahiro Kuchimaru / Kaori Nishikawa / Takayuki Isagawa / Satoshi Iwano / Kei Iida / Hiromasa Hara / Shizuka Miura / Marika Sato / Shigeaki Watanabe / Akifumi Shiomi / Yo Mabuchi / Hiroshi Hamana / Hiroyuki Kishi / Tatsuyuki Sato / Daigo Sawaki / Shigeru Sato / Yutaka Hanazono / Atsushi Suzuki /
    Takahide Kohro / Tetsuya Kadonosono / Tomomi Shimogori / Atsushi Miyawaki / Norihiko Takeda / Hirofumi Shintaku / Shinae Kizaka-Kondoh / Satoshi Nishimura

    Nature Communications, Vol 14, Iss 1, Pp 1-

    2023  Volume 12

    Abstract: Abstract Cancer cells inevitably interact with neighboring host tissue-resident cells during the process of metastatic colonization, establishing a metastatic niche to fuel their survival, growth, and invasion. However, the underlying mechanisms in the ... ...

    Abstract Abstract Cancer cells inevitably interact with neighboring host tissue-resident cells during the process of metastatic colonization, establishing a metastatic niche to fuel their survival, growth, and invasion. However, the underlying mechanisms in the metastatic niche are yet to be fully elucidated owing to the lack of methodologies for comprehensively studying the mechanisms of cell–cell interactions in the niche. Here, we improve a split green fluorescent protein (GFP)-based genetically encoded system to develop secretory glycosylphosphatidylinositol-anchored reconstitution-activated proteins to highlight intercellular connections (sGRAPHIC) for efficient fluorescent labeling of tissue-resident cells that neighbor on and putatively interact with cancer cells in deep tissues. The sGRAPHIC system enables the isolation of metastatic niche-associated tissue-resident cells for their characterization using a single-cell RNA sequencing platform. We use this sGRAPHIC-leveraged transcriptomic platform to uncover gene expression patterns in metastatic niche-associated hepatocytes in a murine model of liver metastasis. Among the marker genes of metastatic niche-associated hepatocytes, we identify Lgals3, encoding galectin-3, as a potential pro-metastatic factor that accelerates metastatic growth and invasion.
    Keywords Science ; Q
    Subject code 610
    Language English
    Publishing date 2023-12-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
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  10. Article ; Online: Heme oxygenase-1: an emerging therapeutic target to curb cardiac pathology.

    Czibik, Gabor / Derumeaux, Geneviéve / Sawaki, Daigo / Valen, Guro / Motterlini, Roberto

    Basic research in cardiology

    2014  Volume 109, Issue 6, Page(s) 450

    Abstract: Activation of heme oxygenase-1 (HO-1), a heme-degrading enzyme responsive to a wide range of cellular stress, is traditionally considered to convey adaptive responses to oxidative stress, inflammation and vasoconstriction. These diversified effects are ... ...

    Abstract Activation of heme oxygenase-1 (HO-1), a heme-degrading enzyme responsive to a wide range of cellular stress, is traditionally considered to convey adaptive responses to oxidative stress, inflammation and vasoconstriction. These diversified effects are achieved through the degradation of heme to carbon monoxide (CO), biliverdin (which is rapidly converted to bilirubin by biliverdin reductase) and ferric iron. Recent findings have added antiproliferative and angiogenic effects to the list of HO-1/CO actions. HO-1 along with its reaction products bilirubin and CO are protective against ischemia-induced injury (myocardial infarction, ischemia-reperfusion (IR)-injury and post-infarct structural remodelling). Moreover, HO-1, and CO in particular, possess acute antihypertensive effects. As opposed to these curative potentials, the long-believed protective effect of HO-1 in cardiac remodelling in response to pressure overload and type 2 diabetes mellitus (DM) has been questioned by recent work. These challenges, coupled with emerging regulatory mechanisms, motivate further in-depth studies to help understand untapped layers of HO-1 regulation and action. The outcomes of these efforts may shed new light on critical mechanisms that could be used to harness the protective potential of this enzyme for the therapeutic benefit of patients suffering from such highly prevalent cardiovascular disorders.
    MeSH term(s) Cardiovascular Diseases/drug therapy ; Cardiovascular Diseases/etiology ; Heme Oxygenase-1/physiology ; Humans
    Chemical Substances Heme Oxygenase-1 (EC 1.14.14.18)
    Language English
    Publishing date 2014
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 189755-x
    ISSN 1435-1803 ; 0300-8428 ; 0175-9418
    ISSN (online) 1435-1803
    ISSN 0300-8428 ; 0175-9418
    DOI 10.1007/s00395-014-0450-9
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