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  • Title: Expression of connective tissue growth factor in acute heart allograft rejection in rats.
    Author: Yuan YC, Xia ZK, Zhang QC, Yin BL.
    Journal: Zhong Nan Da Xue Xue Bao Yi Xue Ban; 2008 May; 33(5):425-31. PubMed ID: 18544847.
    Abstract:
    OBJECTIVE: To detect the expression of connective tissue growth factor (CTGF) in acute heart allograft rejection in rats and to investigate the relationship between CTGF expression and cardiac allograft fibrosis. METHODS: Sixteen Wister rats served as donors and another 16 Sprague-Dawely (SD) rats served as recipients. Intra-abdominal heterotopic heart transplantation was performed. All rats received 10 mg/(kg.d) cyclosporine, 40 mg/(kg.d) CellCept, and 3 mg/(kg.d)methylprednisolone immunosuppression after the surgery. Ten allografts were harvested 2 weeks postoperation while 10 normal Wister rats served as controls. The paraffin sections of harvested heart specimens were stained with hematoxylin and eosin (HE),and van Gieson(VG) for the examination of morphological changes to observe the lumen loss of myocardial coronary arteries and myocardial fibrosis. The expression of CTGF was studied by immunnohistochemical method and was measured semi quantitatively. The correlation between the CTGF expression and allograft fibrosis was studied. RESULTS: The allografts showed a typical symbol of acute rejection with excessive granulocyte infiltration around the vessel wall and myocardial interstice. There were also intimal proliferation and obvious fibrosis in the acute group and the differences between the acute and control group were significant (P< 0.05). The expression of CTGF protein was mainly located around the vascular and myocardial lesions in the acute group while the control group showed no CTGF expression. The gray scale value of CTGF was (AR vs NH: 103.52+/-6.42 vs. 182.61+/-8.72, P< 0.05). Strong negative correlations were found between the gray scale value and fibrosis formation(r=-0.734, P< 0.01). CONCLUSION: CTGF was overexpressed in acute allograft rejection rat hearts and might be involved in the pathogenesis of transplanted heart fibrosis.
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