血管内皮细胞生长因子受体2在慢性静脉性溃疡组织中表达的研究

Expression of VEGFR2 in the tissues of chronic venous ulcer

目的观察静脉性溃疡组织中的血管内皮细胞生长因子受体2(VEGFR2)表达情况,从血管再生障碍途径探讨静脉性溃疡发病机制。方法采用HE染色对比观察溃疡创面组织结构差异;RT-PCR检测VEGFR2mRNA的相对系数;采用免疫组织化学观察CD34、CD133、VEGFR2表达,评估新生血管形成。结果 HE染色见静脉性溃疡创面鳞状上皮结构破坏严重,底部明显附着炎性渗出物。与正常皮肤对照组比较,静脉性溃疡VEGFR-2、CD34、CD133的表达明显降低。采用RT-PCR检测VEGFR2mRNA水平,在病程3周至2个月和大于2个月组中,静脉性溃疡表达相对系数低于创伤溃疡(0.407±0.014、0.249±0.088 vs.0.856±0.049、0.985±0.032),差异有统计学意义(P<0.05)。结论内皮祖细胞(EPCs)的数量和功能受到明显抑制,在损伤局部不能分化形成功能性新生血管,可能是溃疡创面经久不愈的重要原因。

Objective To study expression of VEGFR2 in the tissues of chronic venous ulcer,and to explore pathogenesis of chronic venous ulcer from the pathway of angiogenesis dysfunction. Methods ulcers cell morphology changes were observed with HE staining;VEGFR 2,CD34 and CD133 were detected with immunohistochemistry. The expression of VEGFR2 mRNA was de- tected by RT-PCR. Results HE staining displayed the squamous cell of venous ulcer wound was disarranged, at ulcer base,there was a large number of inflammatory disarranged,at ulcer base,there was a large number of inflammatory exudate. RT-PCR detec- tion of VEGFR2 mRNA content in venous ulcer is lower than the traumatic ulcer group obviously（0. 407 ± 0. 014,0. 249 ± 0. 088 vs. 0. 856±0. 049,0. 985±0. 032,P〈0.05）. Compared with control group,the expression of VEGFR-2,CD34 and CD133 by im- munohistochemistry significantly reduced in venous ulcer. Conclusion The number and function of EPCs was suppressed signifi- cantly, thus the EPCs can not differentiate into functional neovascularizationin in the jury tissues, and that could be important causes of wound that is slow to heal.