Abstract
ObjectivesThe various forms of chronic rejection share a common histological appearance termed allograft arteriosclerosis. In the early stages thereof, apoptosis of vascular smooth muscle cells (VSMC) is obviously reduced, associated with vascular intimal thickening. High-level expression of the HSG/Mfn2 gene promotes apoptosis of rat VSMC. However, the role and mechanism of Mfn2 in inhibition of chronic allograft rejection have not been described. MethodsIn the present study, we transfected transplanted abdominal aortas of donor Lewis rats with an Mfn2-encoding or control lentivirus. And then We transplanted the donor aortas to the corresponding aortal positions in recipient rats. Transplanted aortas were collected on days 30, 60, and 90 and Masson stained to measure intimal thicknesses. Immunohistochemistry would be used to confirm TGF-β1, Mfn2 and TGF-β-R2 expression in different groups. ResultsOur results confirm that high-level expression of Mfn2 lowers the expression of TGF-β1, reduces the intimal thickness of transplanted rat abdominal aorta, and retards the process of chronic rejection. ConclusionMfn2 influences TGF-β/smad pathway and may function as potential chronic rejection inhibitor.
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