Stage-specific functional roles of integrins in murine erythropoiesis

Ulyanova, Tatiana; Padilla, Steven; Papayannopoulou, Thalia

doi:10.1016/j.exphem.2014.01.007

Cited by 20 publications

(31 citation statements)

References 23 publications

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“…Integrin alpha 4 expression declines at a late stage of erythroblast development, leading to the release of these cells from the bone marrow (Ulyanova et al, 2014). The decrease in VCAM1 expression in endothelial cells induced by erythropoietin may also contribute to the release of erythrocytes in response to acute anemia.…”

Section: Discussionmentioning

confidence: 99%

Bone Marrow Endothelial Cells Induce Immature and Mature B Cell Egress in Response to Erythropoietin

Ito

Hamazaki

Takaori‐Kondo³

et al. 2017

Cell Struct. Funct.

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ABSTRACT. Bone marrow stromal cells, including endothelial cells and mesenchymal stromal cells, support the maintenance, differentiation, and retention of hematopoietic stem and precursor cells under steady state conditions. At the onset of an emergency, such as severe blood loss or infection, the status of hematopoiesis in the bone marrow changes rapidly to ensure efficient production of cells of specific lineages; however, the function of stromal cells in emergency hematopoiesis has not been fully elucidated. Here, we unexpectedly found that B precursor, mature B, and T cells were released from the bone marrow into the blood circulation in the early phase of hemorrhagic anemia and phenylhydrazine-induced hemolytic anemia. Administration of erythropoietin, which normally increases in response to anemia, stimulated the egress of IgD low immature B cells and recirculating mature B cells, which usually reside in the perivascular and intravascular space, from the bone marrow within 24 h. We also observed that endothelial cells in the bone marrow expressed erythropoietin receptor, and the expression levels were higher than those in other tissues. Erythropoietin stimulation of bone marrow endothelial cells induced the phosphorylation of STAT5 in vitro. Moreover, in vivo treatment with erythropoietin decreased surface VCAM1 expression and Cxcl12 transcription in bone marrow endothelial cells, both of which are essential for immature and mature B cell retention in the bone marrow. These results suggest that bone marrow endothelial cells can sense and rapidly respond to erythropoietin increase during anemia, thereby regulating B cell emigration from the bone marrow during emergency hematopoiesis.

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Section: Discussionmentioning

confidence: 99%

Bone Marrow Endothelial Cells Induce Immature and Mature B Cell Egress in Response to Erythropoietin

Ito

Hamazaki

Takaori‐Kondo³

et al. 2017

Cell Struct. Funct.

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“…In this model, Dicer is deleted downstream from the CFU-e/proerythroblast stage, when erythropoietin receptor expression begins [13, 16]. Dcr-del mutants were viable, fertile and born in the expected Mendelian ratio.…”

Section: Resultsmentioning

confidence: 99%

“…Single cell suspensions of spleen or freshly isolated bone marrow were stained and analyzed as previously described [15, 16]. …”

Section: Methodsmentioning

confidence: 99%

Deletion of Dicer in late erythroid cells results in impaired stress erythropoiesis in mice

Byon

Padilla

Papayannopoulou

2014

Experimental Hematology

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MicroRNAs (miRNAs) have been shown to influence erythroid lineage commitment and differentiation. However, our knowledge of miRNA function in terminal erythropoiesis remains limited. To address this issue, we generated a novel animal model, where the miRNA-processing enzyme, Dicer, is selectively inactivated in erythropoietin receptor positive erythroid cells beginning with CFU-e/proerythroblast cells. This results in significant depletion of all miRNAs from the proerythroblast stage onwards, with one exception, miR-451, which is processed by Ago2 in a Dicer-independent manner. We observed that mature Dicer-dependent miRNAs, like miR-451, are dispensable under steady-state conditions, but these mutants have an impaired response to stress erythropoiesis, as demonstrated by a delay in recovery from anemia. This defect was specific to later maturing erythroid cells, as progenitor numbers were unaffected. In addition to generating a novel mouse model to study miRNA function in late erythroid cells, we conclude that miRNAs (both Dicer-dependent and independent) act primarily to regulate the optimal response to stress among late erythroid cells.

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“…Some adhesion molecules are under investigation, including integrin β3 (Wang et al, 2013), and integrin α4β1 which is highly expressed on developing erythroblasts and may interact with VCAM-1 present on macrophages (Ulyanova et al, 2014). In addition, focal adhesion kinase (FAK), located downstream of the integrin signaling pathway, has been associated with the stress erythroid response, possibly through mediation of the Epo/STAT5 pathway (Vemula et al, 2010).…”

Section: Pathogenesismentioning

confidence: 99%

β-Thalassemia and Polycythemia vera: Targeting chronic stress erythropoiesis

Crielaard

Rivella

2014

The International Journal of Biochemistry & Cell Biology

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β-thalassemia and Polycythemia vera are genetic disorders which affect the synthesis of red blood cells, also referred to as erythropoiesis. Although essentially different in clinical presentation – patients with β-thalassemia have an impairment in β-globin synthesis leading to defective erythrocytes and anemia, while patients with Polycythemia vera present with high hemoglobin levels because of excessive red blood cell synthesis – both pathologies may characterized by lasting high erythropoietic activity, i.e. chronic stress erythropoiesis. In both diseases, therapeutic strategies targeting chronic stress erythropoiesis may improve the address phenotype and prevent secondary pathology, such as iron overload. The current review will address the basic concepts of these strategies to reduce chronic stress erythropoiesis, which may have significant clinical implications in the near future.

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Stage-specific functional roles of integrins in murine erythropoiesis

Cited by 20 publications

References 23 publications

Bone Marrow Endothelial Cells Induce Immature and Mature B Cell Egress in Response to Erythropoietin

Bone Marrow Endothelial Cells Induce Immature and Mature B Cell Egress in Response to Erythropoietin

Deletion of Dicer in late erythroid cells results in impaired stress erythropoiesis in mice

β-Thalassemia and Polycythemia vera: Targeting chronic stress erythropoiesis

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