Loading…
Exosomes derived from chemically induced human hepatic progenitors inhibit oxidative stress induced cell death
The emerging field of regenerative medicine has revealed that the exosome contributes to many aspects of development and disease through intercellular communication between donor and recipient cells. However, the biological functions of exosomes secreted from cells have remained largely unexplored....
Saved in:
Published in: | Biotechnology and bioengineering 2020-09, Vol.117 (9), p.2658-2667 |
---|---|
Main Authors: | , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | The emerging field of regenerative medicine has revealed that the exosome contributes to many aspects of development and disease through intercellular communication between donor and recipient cells. However, the biological functions of exosomes secreted from cells have remained largely unexplored. Here, we report that the 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 a decrease of cell viability. This event provokes inhibition of caspase dependent cell death signaling, leading to a ROS‐dependent cell damage response and thus induces promotion of antioxidant gene expression or repair of cell death of hypoxia‐exposed cells. Together, these findings show the effect of exosomes in regeneration of liver cells, and offer valuable new insights into liver regeneration.
Protective effect of hCdHs‐derived exosome against oxidative stress in hepatocyte. Exosomes were isolated from chemically induced human hepatic progenitors (hCdHs) by using ‘H’ method. hCdHs‐derived exosome (EXOhCdHs) has a beneficial effect on antioxidant activity of damaged hepatocytes. |
---|---|
ISSN: | 0006-3592 1097-0290 |
DOI: | 10.1002/bit.27447 |