Abstract
In response to elevated glucocorticoid levels, erythroid progenitors rapidly expand to produce large numbers of young erythrocytes. Previous work demonstrates hematopoietic changes in rodents exposed to various physical and psychological stressors, however, the effects of chronic psychological stress on erythropoiesis has not be delineated. We employed laboratory, clinical and genomic analyses of a murine model of chronic restraint stress (RST) to examine the influence of psychological stress on erythropoiesis. Mice exposed to RST demonstrated markers of early erythroid expansion involving the glucocorticoid receptor. In addition, these RST-exposed mice had increased numbers of circulating reticulocytes and increased erythropoiesis in primary and secondary erythroid tissues. Mice also showed increases in erythroid progenitor populations and elevated expression of the erythroid transcription factor KLF1 in these cells. Together this work reports some of the first evidence of psychological stress affecting erythroid homeostasis through glucocorticoid stimulation.
Highlights
Under homeostatic conditions the body produces erythrocytes at a rate sufficient to compensate for normal red blood cell turnover
The microarray revealed a 2.53-fold upregulation in the pre-erythroid transcription factor KLF1 in response to restraint stress (RST) and pathway mapping indicated that that this change in expression could be affected through the glucocorticoid receptor (NR3C1) (Figure 1C)
Restraint stress elevates erythrocyte expression Rodent restraint stress is regularly used in eliciting behavioral and biological symptoms associated with depressive disorders [35,36,37,38]
Summary
Under homeostatic conditions the body produces erythrocytes at a rate sufficient to compensate for normal red blood cell turnover. In response to elevated glucocorticoid levels, erythroid progenitors rapidly expand to produce large numbers of young erythrocytes. This process is subject to the influence of many humoral factors, chief among them are erythropoietin (Epo) and glucocorticoids. Sustained glucocorticoid exposure stimulates proliferation of erythroid progenitors [12,13] and ligand-bound glucocorticoid receptor (GR) acts cooperatively with the transcription factor KLF1 in bi-potent megakaryocyte-erythroid progenitor (MEP) cells to promote terminal erythroid differentiation [14,15,16,17] Taken together, this suggests that sustained elevations in glucocorticoid levels observed in response to psychological stress may enhance erythroid progenitor proliferation and positively influence erythropoiesis
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