Objectives

The 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.

Methods

In 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.

Results

Our 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.

Conclusion

Mfn2 influences TGF-β/smad pathway and may function as potential chronic rejection inhibitor.

中文翻译：

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Mfn2通过调节TGF-β1水平抑制大鼠腹主动脉的慢性排斥反应。

目标

各种形式的慢性排斥反应具有共同的组织学表现，称为同种异体移植动脉硬化。在其早期，血管平滑肌细胞（VSMC）的凋亡明显减少，与血管内膜增厚有关。HSG / Mfn2基因的高水平表达促进大鼠VSMC的凋亡。但是，尚未描述Mfn2在抑制同种异体移植慢性排斥反应中的作用和机制。

方法

在本研究中，我们用Mfn2编码或对照慢病毒转染了供体Lewis大鼠的移植腹主动脉。然后我们将供体主动脉移植到受体大鼠的相应主动脉位置。在第30、60和90天收集移植的主动脉，对Masson染色以测量内膜厚度。免疫组织化学将用于确认不同组中TGF-β1，Mfn2和TGF-β-R2的表达。

结果

我们的结果证实，Mfn2的高水平表达降低了TGF-β1的表达，降低了移植的大鼠腹主动脉的内膜厚度，并延迟了慢性排斥反应的进程。

结论

Mfn2影响TGF-β/ smad途径，并可能充当潜在的慢性排斥抑制剂。