Bennett Laura F, Liao Chang, Paulson Robert F
Department of Veterinary and Biomedical Sciences and Center for Molecular Immunology and Infectious Disease. Laura Bennett and Robert Paulson are Intercollege Graduate Program in Genetics. Robert Paulson and Chang Liao are Pathobiology Graduate Program, The Pennsylvania State University, 115 Henning Building, University Park, PA, 16802, USA.
Methods Mol Biol. 2018;1698:91-102. doi: 10.1007/978-1-4939-7428-3_5.
Bone marrow steady-state erythropoiesis maintains erythroid homeostasis throughout life. This process constantly generates new erythrocytes to replace the senescent erythrocytes that are removed by macrophages in the spleen. In contrast, anemic or hypoxic stress induces a physiological response designed to increase oxygen delivery to the tissues. Stress erythropoiesis is a key component of this response. It is best understood in mice where it is extramedullary occurring in the adult spleen and liver and in the fetal liver during development. Stress erythropoiesis utilizes progenitor cells and signals that are distinct from bone marrow steady-state erythropoiesis. Because of that observation many genes may play a role in stress erythropoiesis despite having no effect on steady-state erythropoiesis. In this chapter, we will discuss in vivo and in vitro techniques to study stress erythropoiesis in mice and how the in vitro culture system can be extended to study human stress erythropoiesis.
骨髓稳态红细胞生成在整个生命过程中维持红细胞内环境稳定。这一过程持续产生新的红细胞，以取代被脾脏中的巨噬细胞清除的衰老红细胞。相比之下，贫血或低氧应激会引发一种旨在增加组织氧输送的生理反应。应激性红细胞生成是这种反应的关键组成部分。在小鼠中对其理解最为透彻，在成年小鼠中，应激性红细胞生成发生在脾脏和肝脏的髓外部位，在发育过程中则发生在胎儿肝脏。应激性红细胞生成利用的祖细胞和信号与骨髓稳态红细胞生成不同。基于这一观察结果，许多基因可能在应激性红细胞生成中发挥作用，尽管它们对稳态红细胞生成没有影响。在本章中，我们将讨论研究小鼠应激性红细胞生成的体内和体外技术，以及如何扩展体外培养系统来研究人类应激性红细胞生成。
