Development of stabilin2+ endothelial cells from mouse embryonic stem cells by inhibition of TGFbeta/activin signaling

Biochemical and Biophysical Research Communications
Hidenori NonakaAtsushi Miyajima

Abstract

To understand the endothelial cell (EC) development, arterial, venous, and lymphatic EC (LEC) have been successfully induced from embryonic stem cells (ESC). However, tissue-specific EC, such as hepatic sinusoidal EC (HSEC), have never been generated from ESC. Based on the findings that TGFbeta/activin signaling negatively regulates differentiation of both LEC and HSEC, and that HSEC and LEC are distinguishable by the expression of marker genes, we assessed the role of TGFbeta/activin signaling in EC development from ESC. Here we show that the inhibition of TGFbeta/activin signaling by a TGFbeta receptor I (TGFbetaRI) kinase inhibitor increased the expression of Lyve1 and stabilin2 but not podoplanin in CD31+CD34+ EC derived from ESC. EC generated by the inhibition of TGFbetaRI signaling also exhibited stronger endocytic activity than control EC, indicating that their phenotype is similar to fetal HSEC. Our results reveal that TGFbeta/activin signaling negatively regulates the early events of HSEC differentiation.

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Citations

Dec 31, 2008·Cell Research·Tetsuro Watabe, Kohei Miyazono
Aug 29, 2013·Future Oncology·Evan WeitmanBabak J Mehrara
Nov 11, 2011·Cell Biology International·Peiliang Wang, Yongbo Cheng
Jan 31, 2012·Journal of Cellular Physiology·Daniel VittetSabine Bailly
Sep 2, 2020·International Journal of Molecular Sciences·Cristina OlgasiAntonia Follenzi
Feb 3, 2012·Physiological Reviews·Kirsty Greenow, Alan R Clarke
Mar 22, 2021·Angiogenesis·Philipp-Sebastian KochHellmut G Augustin

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