TY - JOUR
T1 - TGF-beta-1 up-regulates extra-cellular matrix production in mouse hepatoblasts
AU - Sugiyama, Daisuke
AU - Kulkeaw, Kasem
AU - Mizuochi, Chiyo
N1 - Funding Information:
The authors acknowledge grant support from the Special Coordination Funds for Promoting Science and Technology, a Grant-in-Aid for Young Scientists (B) from The Ministry of Education, Culture, Sports, Science and Technology, a Grant-in-Aid by Ministry of Health, Labor and Welfare, Bilateral Joint Projects for the Japan Society for the Promotion of Science, and the Tokyo Biochemical Research Foundation.
PY - 2013/2
Y1 - 2013/2
N2 - 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.
AB - 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.
UR - https://www.scopus.com/pages/publications/84873526210
UR - https://www.scopus.com/pages/publications/84873526210#tab=citedBy
U2 - 10.1016/j.mod.2012.09.003
DO - 10.1016/j.mod.2012.09.003
M3 - Article
C2 - 23041440
AN - SCOPUS:84873526210
SN - 0925-4773
VL - 130
SP - 195
EP - 206
JO - Mechanisms of Development
JF - Mechanisms of Development
IS - 2-3
ER -