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Lang, R.* ; Hültner, L. ; Lipford, G.B.* ; Wagner, H.* ; Heeg, K.*

Guanosine-rich oligodeoxynucleotides induce proliferation of macrophage progenitors in cultures of murine bone marrow cells.

Eur. J. Immunol. 29, 3496-3506 (1999)
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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Widely used to specifically inhibit gene expression, synthetic oligodeoxynucleotides (ODN)can exert a plethora of non-antisense effects. Immunostimulation by CpG-ODN hasattracted particular attention. ODN rich in the nucleotide guanosine (G-rich ODN) constituteanother type of sequences displaying non-antisense-mediated effects. We have examinedthe effects of CpG- and G-rich ODN on primary mouse bone marrow cells (BMC) in vitro.CpG-ODN induced rapid proliferation of B cells and production of IL-6 and IL-12p40. How-ever, when tested in agar colony assays, CpG-ODN failed to promote the formation of colo-nies. In marked contrast, G-rich non-CpG-ODN led to sustained proliferation ofmacrophage-like cells without inducing cytokines or hemopoietic growth factors. Unlike CpG-ODN, G-rich ODN effectively induced the formation of macrophage colonies in agarassays, indicating a direct action on progenitor cells. Electrophoretic mobility shift assaysrevealed specific binding of G-rich ODN to a non-nuclear protein. The ability of a panel of ODN to compete for binding correlated with their potential to induce proliferation ofmacrophage-like cells from primary mouse BMC. As such, these data reveal a so far unrec-ognized potential of G-rich ODN to signal directly outgrowth of macrophage progenitorsfrom BMC.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Guanosine-rich oligodeoxynucleotides Proliferation Macrophage Bone marrow cell
Sprache englisch
Veröffentlichungsjahr 1999
HGF-Berichtsjahr 1999
ISSN (print) / ISBN 0014-2980
e-ISSN 1521-4141
Quellenangaben Band: 29, Heft: , Seiten: 3496-3506 Artikelnummer: , Supplement: ,
Verlag Wiley
Verlagsort Hoboken
Begutachtungsstatus Peer reviewed
Erfassungsdatum 1999-12-31