Abstract
Phosphatase of regenerating liver-1 (PRL-1) controls various cellular processes and liver regeneration. However, the roles of PRL-1 in liver regeneration induced by chorionic-plate-derived mesenchymal stem cells (CP-MSCs) transplantation remain unknown. Here, we found that increased PRL-1 expression by CP-MSC transplantation enhanced liver regeneration in a bile duct ligation (BDL) rat model by promoting the migration and proliferation of hepatocytes. Engrafted CP-MSCs promoted liver function via enhanced hepatocyte proliferation through increased PRL-1 expression in vivo and in vitro. Moreover, higher increased expression of PRL-1 regulated CP-MSC migration into BDL-injured rat liver through enhancement of migration-related signals by increasing Rho family proteins. The dual effects of PRL-1 on proliferation of hepatocytes and migration of CP-MSCs were substantially reduced when PRL-1 was silenced with siRNA-PRL-1 treatment. These findings suggest that PRL-1 may serve as a multifunctional enhancer for therapeutic applications of CP-MSC transplantation.
Highlights
Despite the liver’s strong regenerative capacity, liver fibrosis and hepatic failure are often caused by various agents, such as inflammation, parasites, metabolic toxins, or drugs, as well as vascular or congenital defects [1,2,3]
Luo et al showed that Phosphatase of regenerating liver-1 (PRL-1) overexpression was associated with elevated levels of matrix metalloproteinases (MMP)-2 and MMP-9 in HEK293 cells through the activation of p130 Cas and focal adhesion kinase (FAK) [19]
We hypothesized that chorionic-plate-derived mesenchymal stem cells (CP-mesenchymal stem cells (MSCs)) homing depends on phosphatase of regenerating liver (PRL)-1 expression, which plays a role in liver regeneration directly or indirectly in a damaged liver
Summary
Despite the liver’s strong regenerative capacity, liver fibrosis and hepatic failure are often caused by various agents, such as inflammation, parasites, metabolic toxins, or drugs, as well as vascular or congenital defects [1,2,3]. Inhibition of PRL-1 expression reduces migration and invasion through c-Src and Rho family GTPases, including Rac and cdc, in cancer cells [17]. Overexpression of PRL-1 induces cell migration ability by regulating the E-cadherin and Rho family GTPases, as well as causing the overexpression of PRL-1, which was observed in metastatic tissue compared to non-metastatic tissue, in consistent agreement with the role of PRL-1 in the regulation of cell migration. Another function of PRL-1 is to promote cell migration and invasion by regulating the matrix metalloproteinases (MMP). Overexpressed PRL-1 expression promotes the increased cell migration and invasion ability via stimulation of MMP-2 and MMP-9 activity [19], which is in agreement with a role of PRL-1 in the regulation of cell migration through gene expression, involved with cell migration
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