Heme oxygenase-1 derived carbon monoxide permits maturation of myeloid cells.

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Heme oxygenase-1 derived carbon monoxide permits maturation of myeloid cells. / Wegiel, Barbara; Hedblom, Andreas; Li, M; Gallo, D; Csizmadia, E; Harris, C; Nemeth, Z; Zuckerbraun, B S; Soares, M; Persson, Jenny L; Otterbein, L E.

I: Cell Death & Disease, Vol. 5, Nr. Mar 20, e1139, 2014.

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

Harvard

Wegiel, B, Hedblom, A, Li, M, Gallo, D, Csizmadia, E, Harris, C, Nemeth, Z, Zuckerbraun, BS, Soares, M, Persson, JL & Otterbein, LE 2014, 'Heme oxygenase-1 derived carbon monoxide permits maturation of myeloid cells.', Cell Death & Disease, vol. 5, nr. Mar 20, e1139. https://doi.org/10.1038/cddis.2014.97

APA

Wegiel, B., Hedblom, A., Li, M., Gallo, D., Csizmadia, E., Harris, C., Nemeth, Z., Zuckerbraun, B. S., Soares, M., Persson, J. L., & Otterbein, L. E. (2014). Heme oxygenase-1 derived carbon monoxide permits maturation of myeloid cells. Cell Death & Disease, 5(Mar 20), [e1139]. https://doi.org/10.1038/cddis.2014.97

CBE

Wegiel B, Hedblom A, Li M, Gallo D, Csizmadia E, Harris C, Nemeth Z, Zuckerbraun BS, Soares M, Persson JL, Otterbein LE. 2014. Heme oxygenase-1 derived carbon monoxide permits maturation of myeloid cells. Cell Death & Disease. 5(Mar 20):Article e1139. https://doi.org/10.1038/cddis.2014.97

MLA

Vancouver

Author

Wegiel, Barbara ; Hedblom, Andreas ; Li, M ; Gallo, D ; Csizmadia, E ; Harris, C ; Nemeth, Z ; Zuckerbraun, B S ; Soares, M ; Persson, Jenny L ; Otterbein, L E. / Heme oxygenase-1 derived carbon monoxide permits maturation of myeloid cells. I: Cell Death & Disease. 2014 ; Vol. 5, Nr. Mar 20.

RIS

TY - JOUR

T1 - Heme oxygenase-1 derived carbon monoxide permits maturation of myeloid cells.

AU - Wegiel, Barbara

AU - Hedblom, Andreas

AU - Li, M

AU - Gallo, D

AU - Csizmadia, E

AU - Harris, C

AU - Nemeth, Z

AU - Zuckerbraun, B S

AU - Soares, M

AU - Persson, Jenny L

AU - Otterbein, L E

PY - 2014

Y1 - 2014

N2 - Critical functions of the immune system are maintained by the ability of myeloid progenitors to differentiate and mature into macrophages. We hypothesized that the cytoprotective gas molecule carbon monoxide (CO), generated endogenously by heme oxygenases (HO), promotes differentiation of progenitors into functional macrophages. Deletion of HO-1, specifically in the myeloid lineage (Lyz-Cre:Hmox1(flfl)), attenuated the ability of myeloid progenitors to differentiate toward macrophages and decreased the expression of macrophage markers, CD14 and macrophage colony-stimulating factor receptor (MCSFR). We showed that HO-1 and CO induced CD14 expression and efficiently increased expansion and differentiation of myeloid cells into macrophages. Further, CO sensitized myeloid cells to treatment with MCSF at low doses by increasing MCSFR expression, mediated partially through a PI3K-Akt-dependent mechanism. Exposure of mice to CO in a model of marginal bone marrow transplantation significantly improved donor myeloid cell engraftment efficiency, expansion and differentiation, which corresponded to increased serum levels of GM-CSF, IL-1α and MCP-1. Collectively, we conclude that HO-1 and CO in part are critical for myeloid cell differentiation. CO may prove to be a novel therapeutic agent to improve functional recovery of bone marrow cells in patients undergoing irradiation, chemotherapy and/or bone marrow transplantation.

AB - Critical functions of the immune system are maintained by the ability of myeloid progenitors to differentiate and mature into macrophages. We hypothesized that the cytoprotective gas molecule carbon monoxide (CO), generated endogenously by heme oxygenases (HO), promotes differentiation of progenitors into functional macrophages. Deletion of HO-1, specifically in the myeloid lineage (Lyz-Cre:Hmox1(flfl)), attenuated the ability of myeloid progenitors to differentiate toward macrophages and decreased the expression of macrophage markers, CD14 and macrophage colony-stimulating factor receptor (MCSFR). We showed that HO-1 and CO induced CD14 expression and efficiently increased expansion and differentiation of myeloid cells into macrophages. Further, CO sensitized myeloid cells to treatment with MCSF at low doses by increasing MCSFR expression, mediated partially through a PI3K-Akt-dependent mechanism. Exposure of mice to CO in a model of marginal bone marrow transplantation significantly improved donor myeloid cell engraftment efficiency, expansion and differentiation, which corresponded to increased serum levels of GM-CSF, IL-1α and MCP-1. Collectively, we conclude that HO-1 and CO in part are critical for myeloid cell differentiation. CO may prove to be a novel therapeutic agent to improve functional recovery of bone marrow cells in patients undergoing irradiation, chemotherapy and/or bone marrow transplantation.

U2 - 10.1038/cddis.2014.97

DO - 10.1038/cddis.2014.97

M3 - Article

C2 - 24651442

VL - 5

JO - Cell Death & Disease

JF - Cell Death & Disease

SN - 2041-4889

IS - Mar 20

M1 - e1139

ER -