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Updated: Apr 28, 2026
Cell Type-specific Gene Expression Profiling in the Mouse Liver
Published on: September 17, 2019
MiR-124 protects human hepatic L02 cells from H2O2-induced apoptosis by targeting Rab38 gene
Xiaohua Li1, Shuhong Yi2, Yinan Deng1
1Liver Surgery Center, 3rd Affiliated Hospital of Sun Yat-sen University, Guangzhou, China; Guangdong Provincial Key Laboratory of Liver Disease Research, Guangzhou, China.
Background:
Hepatic ischemia reperfusion injury (IRI) is an inevitable clinical problem for liver surgeons. Because microRNAs (miRNAs) participate in various hepatic pathophysiological processes, this study aimed to explore the role and potential mechanism of miR-124 in hepatic IRI.
Methods:
A liver IRI model was established in rats. The differential expression of miRNAs was detected using microarrays, and the expression of miR-124 was measured by qRT-PCR. A hydrogen peroxide (H2O2)-induced oxidative stress apoptosis model was also established. Cell apoptosis was detected by flow cytometry, and viability was detected by CCK8. The expression of Rab38 was detected by Western blotting and qRT-PCR, and a luciferase reporter assay was used to verify the expression of the miR-124 target gene.
Results:
The miRNA spectrum changes dramatically after hepatic IRI in rats, and miR-124 is significantly down-regulated after liver IRI. MiR-124 decreases the H2O2-induced apoptosis of human hepatic L02 cells by up-regulating the activation of the AKT pathway. Rab38 is a target gene of miR-124 and is involved in H2O2-induced apoptosis. Interference with the expression of the Rab38 gene can protect hepatic L02 from H2O2-induced apoptosis by increasing the phosphorylation of AKT. These protective effects of miR-124 are attenuated by over-expression of Rab38.
Conclusions:
Many miRNAs are involved in hepatic IRI in rats, and miR-124 is significantly decreased in this model. MiR-124 significantly decreases the H2O2-induced apoptosis of human hepatic L02 cells by targeting the Rab38 gene and activating the AKT pathway.
Insights
MicroRNA-124 (miR-124) is significantly decreased in hepatic ischemia reperfusion injury (IRI). Upregulating miR-124 protects liver cells from apoptosis by targeting Rab38 and activating the AKT pathway.
Area of Science:
- Hepatology
- Molecular Biology
- Cellular Biology
Background:
- Hepatic ischemia reperfusion injury (IRI) presents a significant clinical challenge for liver surgeons.
- MicroRNAs (miRNAs) play crucial roles in various hepatic pathophysiological processes.
- This study investigates the role and mechanism of miR-124 in hepatic IRI.
Purpose of the Study:
- To explore the function of miR-124 in hepatic IRI.
- To elucidate the underlying molecular mechanism of miR-124 in liver injury.
Main Methods:
- Established a rat liver IRI model and a hydrogen peroxide (H2O2)-induced oxidative stress apoptosis model in human hepatic L02 cells.
- Utilized microarrays and qRT-PCR to analyze miRNA expression, focusing on miR-124.
- Employed flow cytometry, CCK8 assays, Western blotting, and luciferase reporter assays to assess apoptosis, cell viability, and gene expression, including the target gene Rab38.
Main Results:
- Hepatic IRI in rats led to significant down-regulation of miR-124.
- Overexpression of miR-124 reduced H2O2-induced apoptosis in L02 cells by upregulating the AKT pathway.
- Rab38 was identified as a direct target gene of miR-124, and its interference protected L02 cells from apoptosis via AKT activation.
Conclusions:
- MiR-124 is significantly decreased in a rat model of hepatic IRI.
- MiR-124 exerts protective effects against H2O2-induced apoptosis in hepatic cells by targeting Rab38 and activating the AKT pathway.
