Exosomes desrived from chemically induced human hepatic progenitors inhibit oxidative stress induced cell death.

The emerging field of regenerative medicine revealed that exosome contributes to many aspects of development and disease through intercellular communication between donor and recipient cells. However, the biological functions of exosome secreted from cells have remained largely unexplored. Here, we report that human hepatic progenitor cells (CdHs)-derived exosome (EXOhCdHs ) plays a crucial role in maintaining cell viability. The inhibition of exosome secretion treatment with GW4869 results in the acceleration of reactive oxygen species (ROS) production, thereby causing the decrease of cell viability. This event provokes inhibition of the caspase dependent cell death signaling, leading to ROS-dependent cell damage response and thus induce promotion of antioxidant gene expression or repair of cell death of hypoxia-exposed cells. Together, these findings provide effect of exosome in regeneration of liver cell, and offer valuable new insights into liver regeneration. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.