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Exosomes derived from chemically induced human hepatic progenitors inhibit oxidative stress induced cell death
Author(s) -
Hyung Sujin,
Jeong Jaemin,
Shin Kyusoon,
Kim Ju Young,
Yim JiHye,
Yu Chan Jong,
Jung Hyun Suk,
Hwang KyungGyun,
Choi Dongho,
Hong Jong Wook
Publication year - 2020
Publication title -
biotechnology and bioengineering
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.136
H-Index - 189
eISSN - 1097-0290
pISSN - 0006-3592
DOI - 10.1002/bit.27447
Subject(s) - microvesicles , microbiology and biotechnology , exosome , progenitor cell , biology , oxidative stress , viability assay , programmed cell death , cytoprotection , regenerative medicine , secretion , stem cell , reactive oxygen species , regeneration (biology) , cell , microrna , apoptosis , biochemistry , gene
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 (EXO hCdHs ) 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.