Journal
MOLECULAR AND CELLULAR BIOCHEMISTRY
Volume 429, Issue 1-2, Pages 113-122Publisher
SPRINGER
DOI: 10.1007/s11010-017-2940-1
Keywords
Liver fibrosis; Human umbilical cord mesenchymal stem cells; Transforming growth factor-beta 1; TGF beta-1/Smad pathway
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Funding
- Youth development projects of Army Medical Technology [15QNP021]
- Medical and Health Research Projects of Army [15MS063]
- Nanjing Science and Technology Development Project [201605061]
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The aim of the current investigation was to evaluate the anti-fibrosis potential of human umbilical cord mesenchymal stem cells (hUC-MSCs) and further to explore some of its underlying mechanisms. Hepatic fibrosis mice model was induced by CCl4. Liver function parameters in serum and fibrosis-associated markers in tissues were detected. Moreover, SB-431542, an anti-TGF beta-1 receptor inhibitor, was employed in vitro to reveal the underlying mechanism of TGF beta-1/Smad pathway on hUC-MSCs against liver fibrosis. In the present study, we illustrated that hUC-MSCs could differentiate into osteogenic, adipogenic, and cartilage. Liver fibrosis was attenuated with hUC-MSCs treatment, determined by reductions of AST, ALT. and fibrosis area, along with some critical parameters including TGF beta-1, alpha-SMA, and TIMP-1. However, TGF beta-1 receptor antagonist SB-431542 reduced the paracrine TGF beta-1 expression of hUC-MSCs and blunted the activation of downstream target genes. Furthermore, the restrained hUC-MSCs proliferation and migration induced by SB-431542 could be reversed by si-TGF beta-1. These results demonstrated that TGF beta-1 receptor inhibitor improved the repair potential of hUC-MSCs against hepatic injury through TGF beta-1/Smad pathway, which contributed to improving the therapeutic efficiency of liver fibrosis.
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