The missing link between proliferation and oxidative stress regulation in hematopoietic stem cells

长期休眠的增殖和对氧化应激的强烈防御反应，防止造血干细胞的衰老和肿瘤发生。在这里，我们表明，GATA 2，造血干细胞的终身维持所必需的转录因子，直接激活几个基因的转录调节细胞增殖，以及调节氧化状态的基因。此外，转录因子Nrf 2缺陷的小鼠，包括调节氧化应激反应基因，表现出不同的动力学的造血干/祖细胞从野生型小鼠。这些结果表明，细胞增殖和抗氧化应激的防御在造血干细胞中具有共同的调节成分。

Long-term dormancy in proliferation and strong defense response against oxidative stresses, prevent the senescence and tumorigenesis of hematopoietic stem cells. Here, we show that GATA2, a transcription factor essential for the life-long maintenance of hematopoietic stem cells, directly activates the transcription of several genes regulating cell proliferation, as well as genes regulating oxidative status. Furthermore, mice deficient in transcription factor Nrf2, which inclusively regulates oxidative stress response genes, show the different kinetics of hematopoietic stem/progenitor cells from wild type mice. These results indicate that cell proliferation and defense against oxidative stresses have shared regulatory components in hematopoietic stem cells.