% pubman genre = article
@article{item_2622983,
title = {{Optimal hypoxia regulates human iPSC-derived liver bud differentiation through intercellular TGFB signaling}},
author = {Ayabe, Hiroaki and Anada, Takahisa and Kamoya, Takuo and Sato, Tomoya and Kimura, Masaki and Yoshizawa, Emi and Kikuchi, Shunyuu and Ueno, Yasuharu and Sekine, Keisuke and Camp, J. Gray and Treutlein, Barbara and Ferguson, Autumn and Suzuki, Osamu and Takebe, Takanori and Taniguchi, Hideki},
language = {eng},
issn = {2213-6711},
doi = {10.1016/j.stemcr.2018.06.015},
publisher = {Cell Press; Elsevier},
address = {Cambridge; New York},
year = {2018},
date = {2018-08-14},
abstract = {{Timely controlled oxygen (O2) delivery is crucial for the developing liver. However, the influence of O2 on intercellular communication during hepatogenesis is unclear. Using a human induced pluripotent stem cell-derived liver bud (hiPSC-LB) model, we found hypoxia induced with an O2-permeable plate promoted hepatic differentiation accompanied by TGFB1 and TGFB3 suppression. Conversely, extensive hypoxia generated with an O2-non-permeable plate elevated TGFBs and cholangiocyte marker expression. Single-cell RNA sequencing revealed that TGFB1 and TGFB3 are primarily expressed in the human liver mesenchyme and endothelium similar to in the hiPSC-LBs. Stromal cell-specific RNA interferences indicated the importance of TGFB signaling for hepatocytic differentiation in hiPSC-LB. Consistently, during mouse liver development, the Hif1a-mediated developmental hypoxic response is positively correlated with TGFB1 expression. These data provide insights into the mechanism that hypoxia-stimulated signals in mesenchyme and endothelium, likely through TGFB1, promote hepatoblast differentiation prior to fetal circulation establishment.}},
journal = {{Stem Cell Reports}},
volume = {11},
number = {2},
pages = {306--316},
}