Pubmed-entry ::= {
  pmid 19569218,
  medent {
    em std {
      year 2010,
      month 2,
      day 22
    },
    cit {
      title {
        name "Modulation of hyaluronan catabolism in chondrocytes by
 mechanical stimuli."
      },
      authors {
        names ml {
          "Tanimoto K",
          "Kitamura R",
          "Tanne Y",
          "Kamiya T",
          "Kunimatsu R",
          "Yoshioka M",
          "Tanaka N",
          "Tanaka E",
          "Tanne K"
        },
        affil str "Department of Orthodontics and Craniofacial Developmental
 Biology, Hiroshima University, Minami-Ku, Hiroshima 734-8553, Japan.
 tkotaro@hiroshima-u.ac.jp"
      },
      from journal {
        title {
          iso-jta "J Biomed Mater Res A",
          ml-jta "J Biomed Mater Res A",
          issn "1552-4965",
          name "Journal of biomedical materials research. Part A"
        },
        imp {
          date std {
            year 2010,
            month 4
          },
          volume "93",
          issue "1",
          pages "373-380",
          language "eng",
          pubstatus ppublish,
          history {
            {
              pubstatus other,
              date std {
                year 2009,
                month 7,
                day 2,
                hour 9,
                minute 0
              }
            },
            {
              pubstatus pubmed,
              date std {
                year 2009,
                month 7,
                day 2,
                hour 9,
                minute 0
              }
            },
            {
              pubstatus medline,
              date std {
                year 2010,
                month 5,
                day 19,
                hour 6,
                minute 0
              }
            }
          }
        }
      },
      ids {
        doi "10.1002/jbm.a.32540",
        pubmed 19569218
      }
    },
    abstract "Hyaluronan (HA) is a component of the extracellular matrices of
 cartilage contributing to the structural and functional integrity. HA
 metabolism is regulated by both anabolic and catabolic processes; however, a
 great deal more of the detail has been unknown yet. The purpose of this study
 was to clarify the effect of excessive mechanical load on the expression and
 activity of hyaluronidase (HYAL) in chondrocytes with a special reference to
 the expressions of IL-1beta and tumor necrosis factor (TNF)-alpha. A cyclic
 tensile load of 22.8% cell elongation, regarded as an excessive mechanical
 stimulus, was applied to cultured rabbit knee articular chondrocytes. HYAL1,
 HYAL2, IL-1beta, and TNF-alpha mRNA levels were examined by quantitative
 real-time PCR analysis. The HYAL activity in culture medium was examined by
 HA zymography. Both HYAL1 and HYAL2 mRNA levels were upregulated
 significantly by the loading in cultured chondrocytes. HYAL activity was also
 enhanced as compared with unloaded controls. The IL-1beta mRNA level was
 upregulated significantly by the loading, and TNF-alpha mRNA level was
 slightly upregulated. HYAL1 and HYAL2 mRNA levels were upregulated
 significantly by IL-1beta treatment, resulting in a slight increase in HYAL
 activity. These results show that the expression of HYAL1 and HYAL2 in
 articular chondrocytes is enhanced by excessive mechanical stimuli and
 affected in part by induction of IL-1beta, leading to HA catabolism in
 articular cartilage.",
    mesh {
      {
        term "Animals"
      },
      {
        term "Cells, Cultured"
      },
      {
        term "Chondrocytes",
        qual {
          {
            subh "enzymology"
          },
          {
            mp TRUE,
            subh "metabolism"
          }
        }
      },
      {
        term "Gene Expression Regulation"
      },
      {
        term "Hyaluronic Acid",
        qual {
          {
            mp TRUE,
            subh "metabolism"
          }
        }
      },
      {
        term "Hyaluronoglucosaminidase",
        qual {
          {
            subh "genetics"
          },
          {
            subh "metabolism"
          }
        }
      },
      {
        term "Inflammation Mediators",
        qual {
          {
            subh "metabolism"
          }
        }
      },
      {
        term "Interleukin-1beta",
        qual {
          {
            subh "genetics"
          },
          {
            subh "metabolism"
          }
        }
      },
      {
        term "Male"
      },
      {
        term "RNA, Messenger",
        qual {
          {
            subh "genetics"
          },
          {
            subh "metabolism"
          }
        }
      },
      {
        term "Rabbits"
      },
      {
        term "Reverse Transcriptase Polymerase Chain Reaction"
      },
      {
        mp TRUE,
        term "Stress, Mechanical"
      },
      {
        term "Tensile Strength"
      },
      {
        term "Tumor Necrosis Factor-alpha",
        qual {
          {
            subh "genetics"
          },
          {
            subh "metabolism"
          }
        }
      }
    },
    substance {
      {
        type nameonly,
        name "Inflammation Mediators"
      },
      {
        type nameonly,
        name "Interleukin-1beta"
      },
      {
        type nameonly,
        name "RNA, Messenger"
      },
      {
        type nameonly,
        name "Tumor Necrosis Factor-alpha"
      },
      {
        type cas,
        cit "9004-61-9",
        name "Hyaluronic Acid"
      },
      {
        type ec,
        cit "3.2.1.35",
        name "Hyaluronoglucosaminidase"
      }
    },
    pmid 19569218,
    pub-type {
      "Journal Article",
      "Research Support, Non-U.S. Gov't"
    },
    status medline
  }
}

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