Overexpression of MyrAkt1 in endothelial cells leads to erythropoietin- and BMP4-independent splenic erythropoiesis in mice

Autor: William C. Aird, Laura E. Benjamin, Whitney E. Goldstein, Carole A. Perruzzi, Rebekah K. O'Donnell
Jazyk: angličtina
Rok vydání: 2013
Předmět:
Mouse
Red Cells
Gene Expression
lcsh:Medicine
Bone Morphogenetic Protein 4
Mice
0302 clinical medicine
Pregnancy
Molecular Cell Biology
Erythropoiesis
lcsh:Science
0303 health sciences
B-Lymphocytes
Multidisciplinary
Chemistry
Anemia
Animal Models
Hematology
Signaling Cascades
Cell biology
Endothelial stem cell
Haematopoiesis
medicine.anatomical_structure
030220 oncology & carcinogenesis
Medicine
Female
Cellular Types
medicine.drug
Research Article
Signal Transduction
Endothelium
Spleen
Bone Marrow Cells
03 medical and health sciences
Model Organisms
Stress
Physiological
medicine
Akt Signaling Cascade
Animals
Humans
Protein kinase B
Erythropoietin
Biology
030304 developmental biology
Blood Cells
lcsh:R
Correction
Endothelial Cells
Hematopoiesis
Immunology
lcsh:Q
Bone marrow
Proto-Oncogene Proteins c-akt
Protein Modification
Translational
Zdroj: PLoS ONE, Vol 8, Iss 1, p e55095 (2013)
PLoS ONE
ISSN: 1932-6203
Popis: Under steady state conditions, erythropoiesis occurs in the bone marrow. However, in mice, stress or tissue hypoxia results in increased erythropoiesis in the spleen. There is increasing evidence that the hematopoietic microenvironment, including endothelial cells, plays an important role in regulating erythropoiesis. Here, we show that short-term expression of constitutively active Akt in the endothelium of mice results in non-anemic stress erythropoiesis in the spleen. The initiation of this stress response was independent of erythropoietin and BMP4, and was observed in endothelial myrAkt1 mice reconstituted with wild-type bone marrow. Together, these data suggest that endothelial cell hyperactivation is a potentially novel pathway of inducing red cell production under stress.
Databáze: OpenAIRE
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