ReferenceID 108
PIN1 Suppresses the Hepatic Differentiation of Pulp Stem Cells via Wnt3a
J Dent Res
This study aimed to investigate the role of PIN1 on the hepatic differentiation of human dental pulp stem cells (hDPSCs) and its signaling pathway, as well as the potential therapeutic effects of hDPSC transplantation an
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Record Fields
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- Reference Id
- 108
- Evidence Id
- 16698
- Core Evidence Id
- 16698
- Source Reference Id
- 182
- Herb2 Reference Id
- HBREF000366
- Subject Paper Key
- HBIN031581_27439725
- Pubmed Id
- 27439725
- Doi
- 10.1177/0022034516659642
- Paper Title
- PIN1 Suppresses the Hepatic Differentiation of Pulp Stem Cells via Wnt3a
- Paper Abstract
- This study aimed to investigate the role of PIN1 on the hepatic differentiation of human dental pulp stem cells (hDPSCs) and its signaling pathway, as well as the potential therapeutic effects of hDPSC transplantation and PIN1 inhibition on CCl4 (carbon tetrachloride)-induced liver fibrosis in mice. The in vitro results showed that hepatic differentiation was suppressed by infection with adenovirus-PIN1 and promoted by PIN1 inhibitor juglone via the downregulation of Wnt3a and β-catenin. Compared with treatment with either hDPSC transplantation or juglone alone, the combination of hDPSCs and juglone into CCl4-injured mice significantly suppressed liver fibrosis and restored serum levels of alanine transaminase, aspartate transaminase, and ammonia. Collectively, the present study shows for the first time that PIN1 inhibition promotes hepatic differentiation of hDPSCs through the Wnt/β-catenin pathway. Furthermore, juglone in combination with hDPSC transplantation effectively treats liver fibrosis, suggesting that hDPSC transplantation with PIN1 inhibition may be a novel therapeutic candidate for the treatment of liver injury.
- Journal
- J Dent Res
- Publish Year
- 2016
- Experiment Subject
- mouse
- Experiment Type
- Animal Experiment
- Phenotype Related
- Paper Title Cn
- Paper Title En
- PIN1 Suppresses the Hepatic Differentiation of Pulp Stem Cells via Wnt3a
- Bilingual Status
- semi_complete