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Liu X, Jia S, Li W, et al. 15-Deoxy-Δ(12,14)-Prostaglandin J2 Inhibits Homing of Bone Marrow-Derived Mesenchymal Stem Cells Triggered by Chronic Liver Injury via Redox Pathway. PPAR Res. 2015;2015:876160doi: 10.1155/2015/876160.
Liu, X., Jia, S., Li, W., Yang, L., Yang, L., Wang, L., & Li, L. (2015). 15-Deoxy-Δ(12,14)-Prostaglandin J2 Inhibits Homing of Bone Marrow-Derived Mesenchymal Stem Cells Triggered by Chronic Liver Injury via Redox Pathway. PPAR research, 2015876160. https://doi.org/10.1155/2015/876160
Liu, Xin, et al. "15-Deoxy-Δ(12,14)-Prostaglandin J2 Inhibits Homing of Bone Marrow-Derived Mesenchymal Stem Cells Triggered by Chronic Liver Injury via Redox Pathway." PPAR research vol. 2015 (2015): 876160. doi: https://doi.org/10.1155/2015/876160
Liu X, Jia S, Li W, Yang L, Yang L, Wang L, Li L. 15-Deoxy-Δ(12,14)-Prostaglandin J2 Inhibits Homing of Bone Marrow-Derived Mesenchymal Stem Cells Triggered by Chronic Liver Injury via Redox Pathway. PPAR Res. 2015;2015:876160. doi: 10.1155/2015/876160. Epub 2015 Sep 20. PMID: 26457076; PMCID: PMC4592740.
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PPAR Res. 2015;2015:876160. doi: 10.1155/2015/876160. Epub 2015 Sep 20.

15-Deoxy-Δ(12,14)-Prostaglandin J2 Inhibits Homing of Bone Marrow-Derived Mesenchymal Stem Cells Triggered by Chronic Liver Injury via Redox Pathway.

PPAR research

Xin Liu, Shuangshuang Jia, Weiyang Li, Le Yang, Lin Yang, Lin Wang, Liying Li

Affiliations

  1. Department of Cell Biology, Municipal Laboratory for Liver Protection and Regulation of Regeneration, Capital Medical University, Beijing 100069, China.

PMID: 26457076 PMCID: PMC4592740 DOI: 10.1155/2015/876160

Abstract

It has been reported that bone marrow-derived mesenchymal stem cells (BMSCs) have capacity to migrate to the damaged liver and contribute to fibrogenesis in chronic liver diseases. 15-Deoxy-Δ(12,14)-prostaglandin J2 (15d-PGJ2), an endogenous ligand for peroxisome proliferator-activated receptor gamma (PPARγ), is considered a new inhibitor of cell migration. However, the actions of 15d-PGJ2 on BMSC migration remain unknown. In this study, we investigated the effects of 15d-PGJ2 on the migration of BMSCs using a mouse model of chronic liver fibrosis and primary mouse BMSCs. Our results demonstrated that in vivo, 15d-PGJ2 administration inhibited the homing of BMSCs to injured liver by flow cytometric analysis and, in vitro, 15d-PGJ2 suppressed primary BMSC migration in a dose-dependent manner determined by Boyden chamber assay. Furthermore, the repressive effect of 15d-PGJ2 was blocked by reactive oxygen species (ROS) inhibitor, but not PPARγ antagonist, and action of 15d-PGJ2 was not reproduced by PPARγ synthetic ligands. In addition, 15d-PGJ2 triggered a significant ROS production and cytoskeletal remodeling in BMSCs. In conclusion, our results suggest that 15d-PGJ2 plays a crucial role in homing of BMSCs to the injured liver dependent on ROS production, independently of PPARγ, which may represent a new strategy in the treatment of liver fibrosis.

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