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Sci Rep. 2015 Feb 27;5:8616. doi: 10.1038/srep08616.

Tonsil-derived mesenchymal stem cells ameliorate CCl4-induced liver fibrosis in mice via autophagy activation.

Author information

1
Department of Microbiology, Ewha Womans University School of Medicine, 1071 Anyangcheon-ro Yangcheon-gu, Seoul, 158-710, Korea.
2
Department of Molecular Medicine, Ewha Womans University School of Medicine, 1071 Anyangcheon-ro Yangcheon-gu, Seoul, 158-710, Korea.
3
1] Department of Otorhinolaryngology-Head and Neck Surgery, Ewha Womans University School of Medicine, 1071 Anyangcheon-ro Yangcheon-gu, Seoul, 158-710, Korea [2] Ewha Global Top 5 Research Program.
4
1] Department of Molecular Medicine, Ewha Womans University School of Medicine, 1071 Anyangcheon-ro Yangcheon-gu, Seoul, 158-710, Korea [2] Ewha Global Top 5 Research Program.
5
Department of Biochemistry, Ewha Womans University School of Medicine, 1071 Anyangcheon-ro Yangcheon-gu, Seoul, 158-710, Korea.
6
1] Department of Pharmaceutics, Ewha Womans University, 52 Ewhayeodae-gil, Seodaemun-gu, Seoul, 120-750, Korea [2] Ewha Global Top 5 Research Program.
7
1] Department of Chemistry and Nano Science, Ewha Womans University, 52 Ewhayeodae-gil, Seodaemun-gu, Seoul, 120-750, Korea [2] Ewha Global Top 5 Research Program.
8
1] Department of Pediatrics, Ewha Womans University School of Medicine, 1071 Anyangcheon-ro Yangcheon-gu, Seoul, 158-710, Korea [2] Ewha Global Top 5 Research Program.

Abstract

Liver transplantation is the treatment of choice for chronic liver failure, although it is complicated by donor shortage, surgery-related complications, and immunological rejection. Cell transplantation is an alternative, minimally invasive treatment option with potentially fewer complications. We used human palatine tonsil as a novel source of mesenchymal stem cells (T-MSCs) and examined their ability to differentiate into hepatocyte-like cells in vivo and in vitro. Carbon tetrachloride (CCl4) mouse model was used to investigate the ability of T-MSCs to home to the site of liver injury. T-MSCs were only detected in the damaged liver, suggesting that they are disease-responsive. Differentiation of T-MSCs into hepatocyte-like cells was confirmed in vitro as determined by expression of hepatocyte markers. Next, we showed resolution of liver fibrosis by T-MSCs via reduction of TGF-β expression and collagen deposition in the liver. We hypothesized that autophagy activation was a possible mechanism for T-MSC-mediated liver recovery. In this report, we demonstrate for the first time that T-MSCs can differentiate into hepatocyte-like cells and ameliorate liver fibrosis via autophagy activation and down-regulation of TGF-β. These findings suggest that T-MSCs could be used as a novel source for stem cell therapy targeting liver diseases.

PMID:
25722117
PMCID:
PMC4342568
DOI:
10.1038/srep08616
[Indexed for MEDLINE]
Free PMC Article

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