Tumor necrosis factor-inducible gene 6 reprograms hepatic stellate cells into stem-like cells, which ameliorates liver damage in mouse.

Abstract:

:Liver fibrosis is a major characteristic of liver disease. When the liver is damaged, quiescent hepatic stellate cells (HSCs) transdifferentiate into proliferative myofibroblastic/activated HSCs, which are the main contributors to liver fibrosis. Hence, a strategy for regulating HSC activation is important in the treatment of liver disease. Tumor necrosis factor-inducible gene 6 protein (TSG-6), a cytokine released from mesenchymal stem cells (MSCs), influences MSC stemness. Therefore, we investigated the biological effect of TSG-6 on HSCs. Human primary HSCs treated with TSG-6 showed significant downregulation of HSC activation markers and upregulation of senescence markers. TSG-6 promoted these cells to express stem cell markers and form spherical organoids, which exhibited elevated expression of stemness-related genes. These organoids differentiated into functional hepatocytic cells under specific culture conditions. Organoids derived from TSG-6-treated HSCs improved livers in organoid transplant mice subjected to CCl4 treatment (which induces liver fibrosis). Furthermore, HSC transdifferentiation by TSG-6 was mediated by Yes-associated protein 1. These findings demonstrate that TSG-6 induces the conversion of HSCs into stem cell-like cells in vitro and that organoids derived from TSG-6-treated HSCs can restore fibrotic liver, suggesting that direct reprogramming of HSCs by TSG-6 can be a useful strategy to control liver disease.

journal_name

Biomaterials

journal_title

Biomaterials

authors

Wang S,Kim J,Lee C,Oh D,Han J,Kim TJ,Kim SW,Seo YS,Oh SH,Jung Y

doi

10.1016/j.biomaterials.2019.119375

subject

Has Abstract

pub_date

2019-10-01 00:00:00

pages

119375

eissn

0142-9612

issn

1878-5905

pii

S0142-9612(19)30474-0

journal_volume

219

pub_type

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