SGT基因在小鼠深静脉血栓形成中的作用

Role of small glutamine-rich tetratricopeptide repeat-containing protein(SGT) in an experimental mouse model of venous thrombosis

目的探讨SGT(small glutamine-rich tetratricopeptide repeat-containing protein)在深静脉血栓(deep vein thrombosis,DVT)形成中的作用。方法分别对SGT基因敲除小鼠及野生型对照鼠进行下腔静脉结扎建立DVT模型,观察建模后两种小鼠体内血栓形成情况,测定出血时间、凝血时间、血栓重量及长度。HE染色观察血栓形成的病理形态特点,ELISA法检测血清中可溶性细胞间黏附分子-1(soluble intercellular adhesion molecule-1,sICAM-1)和白细胞介素-6(interleukin 6,IL-6)的表达。结果与野生型对照鼠相比,SGT基因敲除小鼠在建模48 h后,裸血栓重量长度比明显减小,凝血时间和出血时间均显著延长,形成的血栓中纤维蛋白所占比例较小;SGT基因敲除小鼠血清中sICAM-1表达水平显著低于对照鼠,IL-6的表达水平差异无统计学意义。结论 SGT基因敲除能有效抑制DVT的形成,其作用机制可能与血小板功能受影响及细胞间黏附分子表达改变有关。

Purpose To investigate the role of small glutamine-rich tetratricopeptide repeat-containing protein （SGT） in the thrombotic process in mice. Methods Deep vein thrombosis （DVT） was induced by using an inferior vena cava ligation model in SGT knockout （SGT KO） mice and wild type control mice, respectively. Thrombus formation was assessed by measuring bleeding time, clotting time and the mass weight/length ratio of thrombus specimens. In addition, the thrombus sections were stained with hematoxylin and eosin （HE） for morphometric analysis. The levels of soluble intercellular adhesion molecule-1 （sICAM-1） and interleukin-6 （IL-6） in serum were detected by ELISA. Results As compared with the control mice, bleeding time and clotting time were prolonged and thrombus weight/length ratio was decreased in SGT KO mice with less fibrin composition in the thrombi. The serum level of sICAM-1 was significantly lower in SGT KO mice than in controls, while the IL-6 level showed no significant difference. Conclusion Inhibition of SGT gene expression reduced thrombus formation, which may be related to changed platelet function and expression of intercellular adhesion molecules.