JAK2 V617F 阳性骨髓增殖性肿瘤中的血管生成以及鲁索替尼可降低 JAK2 V617F 阳性细胞中的血管内皮生长因子（VEGF）、缺氧诱导因子-1（HIF-1）的生成。
Angiogenesis in JAK2 V617F positive myeloproliferative neoplasms and ruxolitinib decrease VEGF, HIF-1 enesis in JAK2 V617F positive cells.
作者信息
Cheng Zhiyong, Fu Jianzhu, Liu Guimin, Zhang Lijun, Xu Qian, Wang Su-Yun
机构信息
a Department of Hematology , The No. 1 Hospital of Baoding , Baoding , China.
b Department of Hematology , Hebei General Hospital , Shijiazhuang , Hebei Province , China.
出版信息
Leuk Lymphoma. 2018 Jan;59(1):196-203. doi: 10.1080/10428194.2017.1324155. Epub 2017 May 30.
Angiogenesis and JAK2 V617F mutation are common in BCR-ABL1 negative myeloproliferative neoplasms (MPNs). Ruxolitinib, a JAK inhibitor, is an effective treatment for some MPNs. However, the relationship between angiogenesis and JAK2 V617F and the effects of ruxolitinib on angiogenesis are still unknown. Here, we observed the correlation of JAK2 V617F mutation burden with VEGF, HIF-1a and microvascular density (MVD) in MPNs. We investigate the effect of ruxolitinib on the expression of VEGF and HIF-1α in JAK2 V617F positive cells. We found the expression levels of p-JAK2, VEGF, HIF-1a and MVD in the newly diagnosed MPNs were significantly increased and were related to the JAK2 V617F burden. Ruxolitinib can inhibit p-JAK2, VEGF, HIF-1a expression and suppress blood vessels' formation in chick embryo choriallantoic membrane. Our findings indicated that angiogenesis is related to JAK2 V617F burden and ruxolitinib could decrease VEGF and HIF-1a expression in JAK2 V617F positive cells.
血管生成和JAK2 V617F突变在BCR-ABL1阴性骨髓增殖性肿瘤（MPN）中很常见。鲁索替尼，一种JAK抑制剂，是治疗某些MPN的有效药物。然而，血管生成与JAK2 V617F之间的关系以及鲁索替尼对血管生成的影响仍不清楚。在此，我们观察了MPN中JAK2 V617F突变负荷与VEGF、HIF-1α和微血管密度（MVD）的相关性。我们研究了鲁索替尼对JAK2 V617F阳性细胞中VEGF和HIF-1α表达的影响。我们发现新诊断的MPN中p-JAK2、VEGF、HIF-1α和MVD的表达水平显著升高，且与JAK2 V617F负荷相关。鲁索替尼可抑制p-JAK2、VEGF、HIF-1α的表达，并抑制鸡胚绒毛尿囊膜中的血管形成。我们的研究结果表明，血管生成与JAK2 V617F负荷相关，鲁索替尼可降低JAK2 V617F阳性细胞中VEGF和HIF-1α的表达。
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