PAR1 signaling regulates the retention and recruitment of EPCR-expressing bone marrow hematopoietic stem cells View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-11

AUTHORS

Shiri Gur-Cohen, Tomer Itkin, Sagarika Chakrabarty, Claudine Graf, Orit Kollet, Aya Ludin, Karin Golan, Alexander Kalinkovich, Guy Ledergor, Eitan Wong, Elisabeth Niemeyer, Ziv Porat, Ayelet Erez, Irit Sagi, Charles T Esmon, Wolfram Ruf, Tsvee Lapidot

ABSTRACT

Retention of long-term repopulating hematopoietic stem cells (LT-HSCs) in the bone marrow is essential for hematopoiesis and for protection from myelotoxic injury. We report that signaling cascades that are traditionally viewed as coagulation related also control retention of endothelial protein C receptor-positive (EPCR(+)) LT-HSCs in the bone marrow and their recruitment to the blood via two pathways mediated by protease activated receptor 1 (PAR1). Thrombin-PAR1 signaling induces nitric oxide (NO) production, leading to EPCR shedding mediated by tumor necrosis factor-α-converting enzyme (TACE), enhanced CXCL12-CXCR4-induced motility and rapid stem and progenitor cell mobilization. Conversely, bone marrow blood vessels provide a microenvironment enriched with activated protein C (aPC) that retains EPCR(+) LT-HSCs by limiting NO generation, reducing Cdc42 activity and enhancing integrin VLA4 affinity and adhesion. Inhibition of NO production by aPC-EPCR-PAR1 signaling reduces progenitor cell egress from the bone marrow, increases retention of bone marrow NO(low) EPCR(+) LT-HSCs and protects mice from chemotherapy-induced hematological failure and death. Our study reveals new roles for PAR1 and EPCR in controlling NO production to balance maintenance and recruitment of bone marrow EPCR(+) LT-HSCs, with potential clinical relevance for stem cell transplantation. More... »

PAGES

1307-1317

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nm.3960

    DOI

    http://dx.doi.org/10.1038/nm.3960

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1026450884

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/26457757


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