Aim of the study
This study aimed to investigate the impact of bone marrow-derived mesenchymal stem cell exosomes (BMSC-Exos) on hepatic stellate cell (HSC) activation and explore the underlying molecular mechanisms in liver fibrosis. Material and
Conclusions
BMSC-Exos regulate SLC7A11 expression through miR-144-3p transfer, promoting ferroptosis and suppressing HSC activation in liver fibrosis.
Material and methods
BMSC-Exos were co-incubated with LPS-activated LX-2 cells. Fibrosis markers, iron content, malondialdehyde (MDA), glutathione (GSH), reactive oxygen species (ROS) levels, and ferroptosis-related proteins were assessed. The role of miR-144-3p originating from BMSC-Exos in LX-2 cell activation was studied through dual-luciferase reporter gene and RNA pull-down experiments.
Methods
BMSC-Exos were co-incubated with LPS-activated LX-2 cells. Fibrosis markers, iron content, malondialdehyde (MDA), glutathione (GSH), reactive oxygen species (ROS) levels, and ferroptosis-related proteins were assessed. The role of miR-144-3p originating from BMSC-Exos in LX-2 cell activation was studied through dual-luciferase reporter gene and RNA pull-down experiments.
Results
Treatment with BMSC-Exos up-regulated miR-144-3p in LX-2 cells, down-regulated SLC7A11, increased iron content and ROS levels, and reduced fibrosis markers and GSH. BMSC-Exos mediated ferroptosis and inhibited HSC activation by transmitting miR-144-3p targeting SLC7A11. Conclusions: BMSC-Exos regulate SLC7A11 expression through miR-144-3p transfer, promoting ferroptosis and suppressing HSC activation in liver fibrosis.