Published online Apr 14, 2021. doi: 10.3748/wjg.v27.i14.1419
Peer-review started: October 10, 2020
First decision: January 23, 2021
Revised: February 5, 2021
Accepted: March 7, 2021
Article in press: March 7, 2021
Published online: April 14, 2021
Accumulating evidence has revealed that exosomes play an important role in the progression of metabolic-associated fatty liver disease, but the exact mechanism remains unclear.
Previous studies demonstrated that exosomes from lipotoxic hepatic cells could contribute to hepatic stellate cell (HSC) activation, but the specific cellular crosstalk interaction was not fully illustrated. We aimed to figure out if exosomal microRNA could participate in this procedure.
To determine the role of exosomal miR-1297 in the metabolic-associated fatty liver disease cell model.
miRNA sequencing was conducted to screen differentially-expressed microRNAs. In vitro experiments like quantitative real-time PCR analysis, western blot, immunofluorescence and ethynyl-20-deoxyuridine staining were performed to explore the function of exosomal miR-1297 on HSC activation and proliferation.
miR-1297 was obviously overexpressed in exosomes derived from lipotoxic hepatocytes. The lipotoxic hepatocyte-derived exosomal miR-1297 could promote the activation and proliferation of HSCs through the PTEN/PI3K/AKT signaling pathway.
The lipotoxic hepatocyte-derived exosomal miR-1297 could accelerate the progression of metabolic-associated fatty liver disease in a cell model.
This study provided some new evidence on the crosstalk between hepatocyte-secreted exosomes and HSC. miR-1297 may become a potential target for the treatment of metabolic-associated fatty liver disease.