不同时期血管瘤内皮细胞黏附分子和HLA-DR的表达

目的:探讨黏附分子对血管瘤增殖退化病理生理演变过程的影响及作用机制。方法:应用SABC免疫组化法,检测增殖期血管瘤及退化期血管瘤的细胞间黏附分子-3(Intercellularadhesionmolecule-3,ICAM-3)、CD34和有核细胞表面的组织相容性抗原DR型(Histocompatibilityantigens-DR,HLA-DR)在血管内皮细胞上的表达情况,将2个时期进行比较;同时以血管畸形及正常皮肤为对照。采用行×列表卡方检验进行统计学分析。结果:ICAM-3和CD34均在增殖期血管瘤高表达(分别为26/28和28/28),而退化期低表达或不表达(分别为20/22和20/22),2个时期差异有显著性(P<0.001);而血管畸形和正常皮肤几乎不表达,这与不同时期血管瘤相比差异有显著性(P<0.001);HLA-DR则与血管内皮细胞的高分化阶段密切相关,增殖期基本不表达(4/28),在分化好的退化期高表达(17/22),2个时期差异有显著性(P<0.001)。结论:ICAM-3、CD34可能在血管形成早期发挥作用,介导内皮细胞间黏附,参与血管瘤发病和消退的病理过程。HLA-DR可能与内皮细胞成熟表型的获得及活化状态有关。

Expression of cellular adhesion molecules and HLA-DR antigen on vascular endothelial cells in hemangiomas

PURPOSE: To investigate the expression and function of the adhesion molecules ICAM-3, CD34 and HLA-DR antigen on endothelial cells of hemangiomas in different stages. METHODS: SABC immunohistochemical technique was used to examine the expression of ICAM-3, CD34 and HLA-DR on vascular endothelial cells. Seventy-six specimens including 28 proliferating hemangiomas, 22 involuting hemangiomas, 18 vascular deformity and 8 normal skin tissue were obtained from infants and children for the experiment. RESULTS: The results showed: (1)both ICAM-3 and CD34 had high expression in proliferating hemangiomas, but poor or even no expression in involuting hemangiomas. There was a significant difference (P<0.001) between the two phases. Both ICAM-3 and CD34 had almost no expression in vascular deformity and normal skin tissue, significantly different from hemangiomas (P<0.001).(2)HLA-DR expression was closely related to the high differentiation phase of vascular epithelial cells. In the proliferating phase, HLA-DR didn't express, while it expressed highly as endothelial cells were in well-matured involuting phase. These differences were significant (P<0.001). CONCLUSION: ICAM-3 and CD34 might play a role in the early stage of angiogenesis and take part in the pathological genesis and regression process of hemangiomas by regulating endothelial cells adhesion; HLA-DR might be related either to acquisition of a mature phenotype or to an activated state of the endothelial cells.