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目的探讨基质金属蛋白酶2(MMP-2)、MMP-9在Janus激酶2 V617F(JAK2 V617F)阳性骨髓增殖性肿瘤(MPN)中的表达及意义。方法选取58例JAK2 V617F突变阳性的MPN患者,女24例及男34例,中位年龄57岁。其中包括原发性骨髓纤维化21例、血小板增多症19例、真性红细胞增多症18例。所有58例患者中包括初治组40例(再分为肝或脾肿大组28例及无肝或脾肿大组12例),治疗组18例。对照组为15例健康志愿者。应用免疫组织化学染色法检测各组骨髓组织中磷酸化JAK2(p-JAK2)、MMP-2、MMP-9的表达水平。实时荧光定量PCR方法检测JAK2 V617F与JAK2比值,计算突变量。流式细胞术检测骨髓CD34~+细胞计数。Transwell~(TM)小室检测细胞迁移力。结果 JAK2 V617F/JAK2突变量在初治组高于治疗组,p-JAK2、MMP-2、MMP-9蛋白阳性率在初治组均显著高于治疗组和对照组。Spearman相关分析显示在初治组、治疗组JAK2V617F突变量分别与MMP-2、MMP-9蛋白阳性率正相关。0.5万U/L干扰素α2b(IFN-α2b)能够抑制MPN原代细胞迁移。肝脾肿大组患者JAK2 V617F/JAK2、MMP-2、MMP-9、CD34~+细胞表达水平明显高于无肝脾肿大组。结论 MMP-2、MMP-9在JAK2 V617F阳性MPN中的表达异常升高,并与JAK2 V617F突变量密切相关。
Objective To investigate the expression and significance of MMP-2 and MMP-9 in Janus kinase 2 V617F (JAK2 V617F) positive myeloproliferative neoplasm (MPN). Methods Fifty-eight MPN patients with JAK2 V617F mutation were selected. There were 24 males and 34 males, with a median age of 57 years. Including 21 cases of primary myelofibrosis, 19 cases of thrombocythemia, polycythemia vera 18 cases. All 58 patients included 40 newly diagnosed patients (subdivided into 28 patients with liver or splenomegaly and 12 patients without hepatomegaly or splenomegaly), and 18 patients in the treatment group. The control group was 15 healthy volunteers. Immunohistochemical staining was used to detect the expression of phosphorylated JAK2, MMP-2 and MMP-9 in each group. The ratio of JAK2 V617F to JAK2 was detected by real-time fluorescence quantitative PCR to calculate the mutation amount. Flow cytometry was used to detect the bone marrow CD34 ~ + cell count. Transwell ~ (TM) cells were tested for cell migration. Results The positive rate of JAK2 V617F / JAK2 in the untreated group was higher than that in the untreated group. The positive rates of p-JAK2, MMP-2 and MMP-9 in the untreated group were significantly higher than those in the untreated group and the control group. Spearman correlation analysis showed that in the untreated group, the mutation of JAK2V617F in the treatment group was positively correlated with the positive rate of MMP-2 and MMP-9. 0.5 million U / L interferon alpha 2b (IFN-alpha 2b) was able to inhibit MPN primary cell migration. The expression of JAK2 V617F / JAK2, MMP-2, MMP-9 and CD34 + cells in patients with hepatosplenomegaly were significantly higher than those without hepatosplenomegaly. Conclusion The expression of MMP-2 and MMP-9 in JAK2 V617F positive MPN is abnormally elevated, which is closely related to the mutation of JAK2 V617F.