神经营养酪氨酸激酶受体TrkB在子宫内膜异位症患者在位与异位内膜组织中的表达

目的检测神经营养酪氨酸激酶受体TrkB在正常子宫内膜、子宫内膜异位症（内异症）患者在位和异位内膜组织中的表达，评价TrkB在内异症发病中的作用。方法选择卵巢异位内膜、盆腔腹膜异位内膜和深部浸润结节异位内膜组织（异位内膜组，17例）及子宫在位内膜（在位内膜组，9例，其中4例为增殖期内膜、5例为分泌期内膜）；对照组（9例）为因卵巢良性肿瘤、宫颈病变或浆膜下肌瘤等接受手术治疗的子宫内膜，其中增殖期内膜4例，分泌期内膜5例。RT—PCR技术检测TrkBmRNA的表达量，免疫组化和蛋白免疫印迹法检测TrkB蛋白的表达量。结果（1）对照组内膜组织（增殖期和分泌期）以及在位内膜组（增殖期）不存在TrkBmRNA的表达；在位内膜组（分泌期）和异位内膜组TrkBmRNA的表达分别为（23．51±0．51）％、（35．29±O．67）％，差异有统计学意义（P〈O．05）。（2）免疫组化结果显示，TrkB蛋白的阳性染色主要定位于在位内膜组（分泌期）腺上皮细胞的细胞质（TrkB前体蛋白）、异位内膜组腺上皮细胞的细胞质和部分细胞膜（全长TrkB蛋白）；蛋白免疫印迹结果显示，在位内膜组（分泌期）和异位内膜组TrkB蛋白的表达分别为（0．12±0．02）％和（0．37±0．01）％，差异有统计学意义（P〈0．05）。神经营养酪氨酸激酶受体TrkB在对照组子宫内膜组织中不表达，于在位内膜组（分泌期）和异位内膜组中的表达呈递增趋势。结论神经营养酪氨酸激酶受体TrkB的表达与内异症的发病有关。

Expression of neurotrophic tyrosine kinase receptor TrkB in eutopic and ectopic endometium of women with endometriosis

Objective To investigate the expression of neurotrophic tyrosine kinase receptor TrkB in the eutopic and ectopic endometium of women with endometriosis and evaluate the role of TrkB in the pathogenesis of endometriosis. Methods Seventeen women with endometriosis and 9 controls were studied. Expression of TrkB was investigated using RT-PCR, immunohistochemistry and Western blot, respectively. Results TrkB mRNA was expressed in eutopic endometrium in secretory phase and ectopic endometium of women with endometriosis, （23.51± 0.51 ）% vs （35.29 ±0.67）%（P 〈 0.05）, but TrkB mRNA expression was not detected in control endometrium and eutopic endometrium in proliferative stage of women with endometriosis by RT-PCR. TrkB was expressed both on membrane （glycosylated receptor） and in cytoplasm （non-glycosylated receptor） of the glandular epithelial cells of ectopic endometium, and more often observed in cytoplasm of glandular epithelial cells of eutopic endometrium in secretory phase of women with endometriosis by IHC. In eutopic endometrium in secretory phase and ectopic endometium of women with endometriosis, the expression of TrkB protein was （0.12 ±0.02）% vs （0.37 ±0.01 ）% （P〈 0.05） by Western blot. Conclusions There is an overexpression of TrkB in eutopic endometrium in secretory phase and ectopic endometium of women with endometriosis. Full-length （glycosylated receptor） TrkB more often is overexpressed in ectopic endometium of women with endometriosis, and TrkB may act as a pathogenic role in formation of endometriosis.