Hematopoiesis in Mice in Response to Chronic Hypoxia

Abstract

Exposure to hypoxia results in compensatory processes, including increasing the number of circulating red blood cells and neovascularization, which can increase the efficiency of oxygen delivery, extraction and use. The present study investigated the mechanisms of hematopoiesis in response to chronic hypoxia (10% oxygen exposure) in mice by assessing fluctuations in the peripheral blood cell count, the number of hematopoietic progenitors in the bone marrow and spleen, and serum erythropoietin (EPO) concentrations. Hypoxia induced an exponential increase of serum EPO levels, leading to erythropoiesis. However, no appreciable changes were observed in the number of blood cells, including granulocytes, macrophages, B-lymphocytes and mast cells. The number of fibroblast colony-forming units (CFU-F) in the bone marrow decreased during the first two days, and increased, thereafter, for more than two weeks, suggesting that hypoxic conditions affect the hematopoietic microenvironment cells that are responsible for the regulation of hematopoietic cell proliferation and differentiation.