| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
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| Research Abstract |
Male MSR-A knockout (MSR-A^<-/->) mice and age-matched C57Bl/6J (MSR-A^<+/+>) mice were fed either MCD diet or chow diet for 5 or 15 weeks. Inflammation and fibrosis were determined by tissue staining. Gene expressions were determined by quantitative reverse transcription-PCR (RT-PCR), respectively. MSR-A deficiency attenuated necroinflammatory reaction and macrophage accumulation, as indicated by histopathology and immunohistochemistry for F4/80, in mice fed the MCD diet. This condition reduced the hepatic expression of the proinflammatory genes, such as tumor necrosis factor-alpha, monocyte chemotactic protein 1, and macrophage colony stimulating factor and the profibrogenic genes, such as collagen type I alpha 1, collagen type III alpha 1,α-smooth muscle actin, tissue inhibitor of metalloproteinase-2, and connective tissue growth factor. In addition, MSR-A deficiency significantly reduced collagen deposition in the livers. These results indicate that MSR-A contributes to the augmentation of hepatic inflammation and fibrosis in the mouse model of steatohepatitis.
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