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目的 探讨人脑胶质瘤中层粘连蛋白 (LN)、纤维连接蛋白 (FN)及突变型p5 3基因蛋白的免疫组织化学与肿瘤侵袭微生态系统 (tumorousinvasionmicroecosystem ,TIMES)的相关性。 方法 利用透射电镜观察TIMES中微血管特征和免疫组织化学SP法评价LN、FN、p5 3的表达情况 ,并作比较分析。 结果 1 脑胶质瘤微血管基底膜 (basemembrane ,BM)连续 ,多数呈局限性或广泛性增厚 ,并与LN、FN染色结果相一致 ,也与p5 3染色与否有关 ,p5 3阳性染色者BM增厚较p5 3阴性者明显。 2 LN、FN在所有胶质瘤微血管BM及内皮细胞上呈阳性染色 ,恶性程度越高 ,BM上LN、FN染色阳性越强 ,血管管壁越厚 (P <0 0 1和P <0 0 5 ) ,而瘤细胞未见染色。LN在脑内转移瘤BM和内皮细胞上却未见染色 ,但可见散在瘤细胞浆膜染色 ;FN在脑内转移瘤上的染色则与脑胶质瘤相类似。 3 45例胶质瘤中p5 3阳性染色 2 1例 ,其p5 3阳性染色与否也与BM上LN、FN染色结果存在密切正相关 (P <0 0 1)。p5 3阳性染色率在脑内转移瘤和恶性胶质瘤中无统计学差别 (P >0 0 5 )。 结论 脑微血管内皮细胞上LN、FN的过分表达可能是脑胶质瘤TIMES中BM形态学增厚的原因之一 ,p5 3对TIMES的影响也与微血管的内皮细胞功能状态有关。血管内皮细胞可能是TIMES的调控?
Objective To investigate the relationship between immunohistochemistry and tumorous invasion microecosystem (TIMES) of laminin (LN), fibronectin (FN) and mutant p5 3 in human glioma. Methods The microvessel characteristics of TIMES were observed by transmission electron microscopy and the expression of LN, FN and p5 3 were evaluated by immunohistochemical SP method and compared. Results 1 The glomerulus basement membrane basement membrane (basemembrane, BM) was continuous, mostly localized or extensive thickening, consistent with the results of LN, FN staining, but also with p5 3 staining or not, p5 3 positive staining BM thickened more than p5 3 negative. LN and FN were positive staining in all glioma microvasculature BM and endothelial cells. The higher the degree of malignancy, the stronger the LN and FN staining on BM, the thicker the vascular wall (P <0.01 and P <0 0) 5), while no staining of tumor cells. LN in brain metastases BM and endothelial cells but no staining, but scattered in the plasma membrane staining; FN in brain metastases staining and glioma is similar. There was a positive correlation between p5 3 positive staining and LN and FN staining on BM (P <0.01) in 451 cases of p5 3 positive staining in gliomas. The positive staining rate of p5 3 in brain metastases and gliomas was not statistically different (P> 0.05). Conclusion The overexpression of LN and FN on brain microvascular endothelial cells may be one of the causes of BM hypertrophy in TIMES. The effect of p5 3 on TIMES is also related to the functional status of endothelial cells in microvessels. Vascular endothelial cells may be TIMES regulation?