Adipose-derived mesenchymal stem cells inhibit activation of hepatic stellate cells in vitro and ameliorate rat liver fibrosis in vivo

Background/purpose Previous studies suggested that mesenchymal stem cells may ameliorate fibrogenesis through the inhibition of hepatic stellate cells (HSCs) activation. This study aimed to investigate whether adipose derived mesenchymal stem cells (ADSCs) could modulate the activation of HSCs and c...

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Published in:Journal of the Formosan Medical Association 2015-02, Vol.114 (2), p.130-138
Main Authors: Yu, Fuxiang, Ji, Shiqiang, Su, Longfeng, Wan, Li, Zhang, Shengchu, Dai, Chunlei, Wang, Yang, Fu, Junhui, Zhang, Qiyu
Format: Article
Language:English
Subjects:
Actins - metabolism
adipose derived mesenchymal stem cells
Adipose Tissue - cytology
Animals
Apoptosis
Carbon Tetrachloride
Cell Proliferation
Cells, Cultured
fibrosis
hepatic stellate cells
Hepatic Stellate Cells - cytology
Internal Medicine
Liver - pathology
Liver Cirrhosis - chemically induced
Liver Cirrhosis - therapy
Male
Mesenchymal Stem Cell Transplantation
Mesenchymal Stromal Cells - cytology
proliferation
Rats
Rats, Sprague-Dawley
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Summary:Background/purpose Previous studies suggested that mesenchymal stem cells may ameliorate fibrogenesis through the inhibition of hepatic stellate cells (HSCs) activation. This study aimed to investigate whether adipose derived mesenchymal stem cells (ADSCs) could modulate the activation of HSCs and contribute to the recovery of liver fibrogenesis. Methods ADSCs and HSCs were isolated from Sprague-Dawley rats and co-cultured using a transwells insert. Cell proliferation, apoptosis and smooth muscle α-actin (α-SMA) expression in HSCs were examined. Rats were injected with CCl4 to induce liver fibrogenesis. After injection of ADSCs through portal vein, the rats were examined for pathological changes in the liver. α-SMA expression and hydroxyproline content in the liver and serum levels of collagen III and hyaluronic acid was detected. Results After co-culturing for 72 h, the proliferation and activation of HSCs was inhibited by ADSCs and the apoptosis of HSCs was promoted by ADSCs. Transplantation of ADSCs inhibited liver fibrogenesis in the rats. Conclusion ADSCs inhibit the proliferation and activation of HSCs in vitro and inhibit liver fibrogenesis in rat model, suggesting the potential application of ADSCs in liver fibrogenesis therapy.
ISSN:0929-6646
DOI:10.1016/j.jfma.2012.12.002