Fibroblast Growth Factor-5 Participates in the Progression of Hepatic Fibrosis

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Author(s)

    • HANAKA Hiromi Hanaka Hiromi
    • Department of Developmental Anatomy and Regenerative Biology, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan
    • ITO Masataka [他] Ito Masataka
    • Department of Developmental Anatomy and Regenerative Biology, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan
    • Nakashima Hiroyuki
    • Department of Immunology and Microbiology, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan
    • Tomita Kengo
    • Division of Gastroenterology and Hepatology, Department of Internal Medicine, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan
    • Seki Shuhji
    • Department of Immunology and Microbiology, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan
    • Kobayashi Yasushi
    • Department of Anatomy and Neurobiology, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan
    • Imaki Junko
    • Department of Developmental Anatomy and Regenerative Biology, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan

Abstract

Non-alcoholic steatohepatitis (NASH) is characterized by the presence of steatosis, inflammation, and fibrosis and is believed to develop via a “two-hit process”; however, its pathophysiology remains unclear. Fibroblast growth factors (FGFs) are heparin-binding polypeptides with diverse biological activities in many developmental and metabolic processes. In particular, FGF5 is associated with high blood pressure. We investigated the function of FGF5 <i>in vivo</i> using spontaneously Fgf5 null mice and explored the role of diet in the development of NASH. Mice fed a high-fat diet gained little weight and had higher serum alanine transaminase, aspartate amino transferase, and non-high-density lipoprotein-cholesterol levels. Liver histology indicated marked inflammation, focal necrosis, fat deposition, and fibrosis, similar to the characteristics of NASH. FGF5 and a high-fat diet play significant roles in the pathophysiology of hepatic fibrosis and Fgf5 null mice may provide a suitable model for liver fibrosis or NASH.

Journal

  • Experimental Animals

    Experimental Animals 63(1), 85-92, 2014

    Japanese Association for Laboratory Animal Science

Codes

  • NII Article ID (NAID)
    130003391608
  • NII NACSIS-CAT ID (NCID)
    AA11032321
  • Text Lang
    ENG
  • ISSN
    1341-1357
  • NDL Article ID
    025152819
  • NDL Call No.
    Z54-H752
  • Data Source
    NDL  J-STAGE 
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