TGF-beta-1 up-regulates extra-cellular matrix production in mouse hepatoblasts

Daisuke Sugiyama, Kasem Kulkeaw, Chiyo Mizuochi

Research output: Contribution to journalArticlepeer-review

30 Citations (Scopus)


Fetal liver is the major embryonic hematopoietic organ and is extrinsically colonized by circulating hematopoietic stem cells (HSCs). Integrin beta-1 expression on HSCs is crucial for colonization, suggesting that interaction of Integrin beta-1 with extra-cellular matrix (ECM) factors promotes HSC adherence to fetal liver. However, little is known about how ECM production is regulated in fetal liver. Here we used flow cytometry to sort fetal liver compartments and detected ECM gene and protein expression predominantly in sorted hepatoblasts. mRNA and protein analysis suggested that TGF-beta-1 expressed by hepatoblasts, sinusoid endothelial cells and hematopoietic cells, binds to the TGF-beta receptor type-2 expressed on hepatoblasts to stimulate ECM production. Intra-cardiac injection of TGF-inhibitors into mouse embryos dramatically decreased fetal liver ECM gene expression. Taken together, our observations suggest that hepatoblasts predominantly produce ECM factors under control of TGF-beta-1 in fetal liver.

Original languageEnglish
Pages (from-to)195-206
Number of pages12
JournalMechanisms of Development
Issue number2-3
Publication statusPublished - Feb 2013
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Embryology
  • Developmental Biology


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