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Neutralization of CXCL10 accelerates liver regeneration in carbon tetrachloride-induced acute liver injury.

Neutralization of CXCL10 accelerates liver regeneration in carbon tetrachloride-induced acute liver injury. Research Abstract Details 

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  • Neutralization of CXCL10 accelerates liver regeneration in carbon tetrachloride-induced acute liver injury. Abstract Text:

    hiroyuki yoneyamaHiroyuki Yoneyama,yoshiro kaiYoshiro Kai,jun koyamaJun Koyama,kenji suzukiKenji Suzuki,hiroshi kawachiHiroshi Kawachi,shosaku narumiShosaku Narumi,takafumi ichidaTakafumi Ichida,hiroyuki yoneyamaHiroyuki Yoneyama,yoshiro kaiYoshiro Kai,jun koyamaJun Koyama,kenji suzukiKenji Suzuki,hiroshi kawachiHiroshi Kawachi,shosaku narumiShosaku Narumi,takafumi ichidaTakafumi Ichida,

    Remodeling of hepatic tissue structure following injury requires the coordinated action of hepatocytes, hepatic stellate cells (HSCs), and endothelial cells. However, their in vivo properties are not fully understood. We report here that the chemokine CXCL10 regulates hepatic tissue remodeling in a carbon tetrachloride (CCl(4))-induced acute liver injury in mice. The production of CXCL10 was enhanced by hepatocytes after CCl(4) exposure. Neutralization of CXCL10 protected mice from acute liver dysfunction and diminished hepatocellular loss. The hepatoprotective effect was associated with increased numbers of 5'-bromo-2' deoxyuridine (BrdU)+ hepatocytes from day 1 and with accumulation of HSCs and endothelial cells within the injured zones from day 3. In vitro, recombinant CXCL10 directly inhibited the proliferation of hepatocytic cells, establishing a novel role of CXCL10 in modulating hepatocyte proliferation, in addition to a previously reported angiostatic role. In summary, neutralization of CXCL10 initially stimulates hepatocyte proliferation and, subsequently, HSC migration and angiogenesis to facilitate remodeling of hepatic cords. Thus, CXCL10 can be a novel therapeutic target for acute hepatocellular damage by regulating liver tissue remodeling.

    Neutralization of CXCL10 accelerates liver regeneration in carbon tetrachloride-induced acute liver injury. Publishing Authors By Initials

    h yoneyamaH Yoneyama,y kaiY Kai,j koyamaJ Koyama,k suzukiK Suzuki,h kawachiH Kawachi,s narumiS Narumi,t ichidaT Ichida,h yoneyamaH Yoneyama,y kaiY Kai,j koyamaJ Koyama,k suzukiK Suzuki,h kawachiH Kawachi,s narumiS Narumi,t ichidaT Ichida,

    For similar abstracts research abstracts see: abstracts research

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    Neutralization of CXCL10 accelerates liver regeneration in carbon tetrachloride-induced acute liver injury. Journal Published:

    PUBLICATION TYPE: Journal Article

    Journal: Medical molecular morphology

    VOLUME: 40

    Page Numbers: 191-7

    Journal Abbreviation:

    ISSN: 1860-1480

    DAY: 21

    MONTH: 12

    YEAR: 2007

    Neutralization of CXCL10 accelerates liver regeneration in carbon tetrachloride-induced acute liver injury. Information

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    LANGUAGE: eng

    NlmUniqueID: 101239023

    Neutralization of CXCL10 accelerates liver regeneration in carbon tetrachloride-induced acute liver injury. Keywords Mesh Terms:

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    Grant and Affiliation Information for Neutralization of CXCL10 accelerates liver regeneration in carbon tetrachloride-induced acute liver injury.

    AFFILIATION: Laboratory of Stem Cell Dynamism, Stelic Institute of Regenerative Medicine, Stelic Institute & Co., 1-9-15 Higashi-azabu, Mihato-ku, Tokyo, 106-0044, Japan, yoneyama@stelic.co.jp.

    Country: Japan

    Japan Research PublicationJapan Research Publication

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    MEDLINETA: Med Mol Morphol

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