Role of the angiotensin-converting enzyme in the G-CSF-induced mobilization of progenitor cells View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2018-05

AUTHORS

Karin Kohlstedt, Caroline Trouvain, Timo Frömel, Thomas Mudersbach, Reinhard Henschler, Ingrid Fleming

ABSTRACT

In addition to being a peptidase, the angiotensin-converting enzyme (ACE) can be phosphorylated and involved in signal transduction. We evaluated the role of ACE in granulocyte-colony-stimulating factor (G-CSF)-induced hematopoietic progenitor cell (HPC) mobilization and detected a significant increase in mice-lacking ACE. Transplantation experiments revealed that the loss of ACE in the HPC microenvironment rather than in the HPCs increased mobilization. Indeed, although ACE was expressed by a small population of bone-marrow cells, it was more strongly expressed by endosteal bone. Interestingly, there was a physical association of ACE with the G-CSF receptor (CD114), and G-CSF elicited ACE phosphorylation on Ser1270 in vivo and in vitro. A transgenic mouse expressing a non-phosphorylatable ACE (ACES/A) mutant demonstrated increased G-CSF-induced HPC mobilization and decreased G-CSF-induced phosphorylation of STAT3 and STAT5. These results indicate that ACE expression/phosphorylation in the bone-marrow niche interface negatively regulates G-CSF-induced signaling and HPC mobilization. More... »

PAGES

18

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00395-018-0677-y

DOI

http://dx.doi.org/10.1007/s00395-018-0677-y

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1101550243

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29549541


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