Gilles Laure, Arslan Ahmet Dirim, Marinaccio Christian, Wen Qiang Jeremy, Arya Priyanka, McNulty Maureen, Yang Qiong, Zhao Jonathan C, Konstantinoff Katerina, Lasho Terra, Pardanani Animesh, Stein Brady, Plo Isabelle, Sundaravel Sriram, Wickrema Amittha, Migliaccio Annarita, Gurbuxani Sandeep, Vainchenker William, Platanias Leonidas C, Tefferi Ayalew, Crispino John D
J Clin Invest. 2017 Apr 3;127(4):1316-1320. doi: 10.1172/JCI82905. Epub 2017 Feb 27.
Primary myelofibrosis (PMF) is a clonal hematologic malignancy characterized by BM fibrosis, extramedullary hematopoiesis, circulating CD34+ cells, splenomegaly, and a propensity to evolve to acute myeloid leukemia. Moreover, the spleen and BM of patients harbor atypical, clustered megakaryocytes, which contribute to the disease by secreting profibrotic cytokines. Here, we have revealed that megakaryocytes in PMF show impaired maturation that is associated with reduced GATA1 protein. In investigating the cause of GATA1 downregulation, our gene-expression study revealed the presence of the RPS14-deficient gene signature, which is associated with defective ribosomal protein function and linked to the erythroid lineage in 5q deletion myelodysplastic syndrome. Surprisingly, reduced GATA1 expression and impaired differentiation were limited to megakaryocytes, consistent with a proproliferative effect of a GATA1 deficiency on this lineage. Importantly, expression of GATA1 effectively rescued maturation of PMF megakaryocytes. Together, these results suggest that ribosomal deficiency contributes to impaired megakaryopoiesis in myeloproliferative neoplasms.
原发性骨髓纤维化(PMF)是一种克隆性血液系统恶性肿瘤,其特征为骨髓纤维化、髓外造血、循环CD34+细胞、脾肿大以及易演变为急性髓系白血病。此外,患者的脾脏和骨髓中存在非典型的聚集巨核细胞,这些细胞通过分泌促纤维化细胞因子促进疾病发展。在此,我们发现PMF中的巨核细胞成熟受损,这与GATA1蛋白减少有关。在研究GATA1下调的原因时,我们的基因表达研究揭示了RPS14缺陷基因特征的存在,该特征与核糖体蛋白功能缺陷相关,并与5q缺失骨髓增生异常综合征中的红系谱系有关。令人惊讶的是,GATA1表达降低和分化受损仅限于巨核细胞,这与GATA1缺乏对该谱系的促增殖作用一致。重要的是,GATA1的表达有效地挽救了PMF巨核细胞的成熟。总之,这些结果表明核糖体缺陷导致骨髓增殖性肿瘤中巨核细胞生成受损。