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Adiponectin modulates inflammatory reactions via calreticulin receptor-dependent clearance of early apoptotic bodies.

Adiponectin modulates inflammatory reactions via calreticulin receptor-dependent clearance of early apoptotic bodies. Research Abstract Details 

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  • Adiponectin modulates inflammatory reactions via calreticulin receptor-dependent clearance of early apoptotic bodies. Abstract Text:

    yukihiro takemuraYukihiro Takemura,noriyuki ouchiNoriyuki Ouchi,rei shibataRei Shibata,tamar aprahamianTamar Aprahamian,michael t kirberMichael T Kirber,ross s summerRoss S Summer,shinji kiharaShinji Kihara,kenneth walshKenneth Walsh,

    Obesity and type 2 diabetes are associated with chronic inflammation. Adiponectin is an adipocyte-derived hormone with antidiabetic and antiinflammatory actions. Here, we demonstrate what we believe to be a previously undocumented activity of adiponectin, facilitating the uptake of early apoptotic cells by macrophages, an essential feature of immune system function. Adiponectin-deficient (APN-KO) mice were impaired in their ability to clear apoptotic thymocytes in response to dexamethasone treatment, and these animals displayed a reduced ability to clear early apoptotic cells that were injected into their intraperitoneal cavities. Conversely, adiponectin administration promoted the clearance of apoptotic cells by macrophages in both APN-KO and wild-type mice. Adiponectin overexpression also promoted apoptotic cell clearance and reduced features of autoimmunity in lpr mice whereas adiponectin deficiency in lpr mice led to a further reduction in apoptotic cell clearance, which was accompanied by exacerbated systemic inflammation. Adiponectin was capable of opsonizing apoptotic cells, and phagocytosis of cell corpses was mediated by the binding of adiponectin to calreticulin on the macrophage cell surface. We propose that adiponectin protects the organism from systemic inflammation by promoting the clearance of early apoptotic cells by macrophages through a receptor-dependent pathway involving calreticulin.

    Adiponectin modulates inflammatory reactions via calreticulin receptor-dependent clearance of early apoptotic bodies. Publishing Authors By Initials

    y takemuraY Takemura,n ouchiN Ouchi,r shibataR Shibata,t aprahamianT Aprahamian,mt kirberMT Kirber,rs summerRS Summer,s kiharaS Kihara,k walshK Walsh,

    For similar proteins: recombinant proteins research abstracts see: proteins: recombinant proteins research

    PUBMED ID PMID:

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    Adiponectin modulates inflammatory reactions via calreticulin receptor-dependent clearance of early apoptotic bodies. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: The Journal of clinical investigation

    VOLUME: 117

    Page Numbers: 375-86

    Journal Abbreviation: J. Clin. Invest.

    ISSN: 0021-9738

    DAY: 25

    MONTH: 01

    YEAR: 2007

    Adiponectin modulates inflammatory reactions via calreticulin receptor-dependent clearance of early apoptotic bodies. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 7802877

    Adiponectin modulates inflammatory reactions via calreticulin receptor-dependent clearance of early apoptotic bodies. Keywords Mesh Terms:

    KEYWORDS: Recombinant Proteins

    MESH TERMS: pharmacology

    Chemical & Substance for Abstract: Adiponectin modulates inflammatory reactions via calreticulin receptor-dependent clearance of early apoptotic bodies. Information

    Substance Name: adiponectin, mouse

    Registry Number: 0

    Grant and Affiliation Information for Adiponectin modulates inflammatory reactions via calreticulin receptor-dependent clearance of early apoptotic bodies.

    AFFILIATION: Molecular Cardiology Unit, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts 02118, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: N01-HV-28178

    ACRONYM: HV

    MEDLINETA: J Clin Invest

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

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