Hepatic differentiation induced by oncostatin M attenuates fetal liver hematopoiesis

Taisei Kinoshita, Takashi Sekiguchi, Ming Jiang Xu, Yoshiaki Ito, Akihide Kamiya, Koh Ichiro Tsuji, Tatsutoshi Nakahata, Atsushi Miyajima

Research output: Contribution to journalArticle

146 Scopus citations

Abstract

Embryonic liver is a transient site for definitive hematopoiesis. Along with maturation of the bone marrow and spleen, hematopoietic cells relocate from the liver to their final destinations while the liver starts organizing its own structure and develops numerous metabolic functions toward adult. Recently, it was demonstrated that the signal exerted by oncostatin M (OSM) through gp130 plays a pivotal role in the maturation process of the liver both in vitro and in vivo. However, the molecular basis underlying the termination of embryonic hematopoiesis remains unknown. In this study, we report that primary culture of fetal hepatic cells from embryonic day 14.5 murine embryos supported expansion of blood cells from Lin-Sca-1+c-Kit+ cells, giving rise to myeloid, lymphoid, and erythroid lineages. Of interest, promotion of hepatic development by OSM and glucocorticoid strongly suppressed in vitro hematopoiesis. Consistent with these results, hepatic culture from the embryonic day 18.5 liver no longer supported hematopoiesis. These data together with the previous observations suggest that the signals exerted by OSM and glucocorticoid induce hepatic differentiation, which in turn terminate embryonic hematopoiesis and promote relocation of hematopoietic cells.

Original languageEnglish (US)
Pages (from-to)7265-7270
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume96
Issue number13
DOIs
StatePublished - Jun 22 1999
Externally publishedYes

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