Format

Send to

Choose Destination

Links from PubMed

See comment in PubMed Commons below
PLoS One. 2013;8(1):e55095. doi: 10.1371/journal.pone.0055095. Epub 2013 Jan 28.

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

Author information

  • 1Department of Pathology, Beth Israel Deaconess Medical Center, Boston, MA, USA. rebekah.k.odonnell@gmail.com

Erratum in

  • PLoS One. 2013;8(6). doi: 10.1371/annotation/207f3e91-451e-4508-afab-77f01dae3fe9. Aird, William [corrected to Aird, William C].

Abstract

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.

[PubMed - indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Public Library of Science Icon for PubMed Central
    Loading ...
    Write to the Help Desk