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Published on: January 10, 2025
[The miR-148a alleviates hepatic ischemia/reperfusion injury in mice via targeting CaMKIIα]
Daofeng Zheng1, Diao He1, Xiuxian Lu1
1Department of Hepatobiliary Surgery, First Affiliated Hospital, Chongqing Medical University, Chongqing 400016, China.
Abstract:
Objective To evaluate the impact of miR-148a on hepatic ischemia/reperfusion (I/R) injury via inhibiting Ca(2+)/calmodulin-dependent protein kinase IIα (CaMKIIα), and analyze the potential mechanism. Methods Liver I/R model was built in mice. Expression of CaMKIIα was detected in the hepatic tissues by Western blotting. The mRNA levels of miR-148a, CaMKIIα, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were analyzed by quantitative real-time PCR (qRT-PCR). HE staining was performed to observe morphological changes of the livers in each group. TUNEL was used to evaluate the degree of hepatocellular apoptosis in each group. Results After hepatic I/R injury, the expression of miR-148a increased, and it was negatively correlated with CaMKIIα. After therapy with exogenous miR-148a mimics, the protein expression of CaMKIIα, the mRNA levels of TNF-α and IL-1β, the degree of inflammatory cell infiltration and liver cell necrosis, and the level of hepatocellular apoptosis were all downregulated. Conclusion The miR-148a may alleviate hepatic I/R injury in mouse by inhibiting CaMKIIα.
Insights
MicroRNA-148a (miR-148a) can reduce liver injury caused by ischemia/reperfusion (I/R). This study shows miR-148a alleviates hepatic I/R injury by inhibiting Ca(2+)/calmodulin-dependent protein kinase IIα (CaMKIIα).
Area of Science:
- Hepatology
- Molecular Biology
- Immunology
Background:
- Hepatic ischemia/reperfusion (I/R) injury is a significant clinical challenge.
- MicroRNAs (miRNAs) play crucial roles in regulating cellular processes, including injury responses.
- Ca(2+)/calmodulin-dependent protein kinase IIα (CaMKIIα) is implicated in various cellular signaling pathways.
Purpose of the Study:
- To investigate the role of miR-148a in hepatic I/R injury.
- To determine if miR-148a exerts its effects by inhibiting CaMKIIα.
- To elucidate the underlying molecular mechanisms.
Main Methods:
- Establishment of a mouse model for hepatic I/R injury.
- Quantitative real-time PCR (qRT-PCR) to measure mRNA levels of miR-148a, CaMKIIα, TNF-α, and IL-1β.
- Western blotting to assess CaMKIIα protein expression.
- Hematoxylin and eosin (HE) staining for histological evaluation.
- Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay for apoptosis assessment.
Main Results:
- Hepatic I/R injury led to increased miR-148a expression, negatively correlated with CaMKIIα.
- Administration of miR-148a mimics downregulated CaMKIIα protein expression.
- miR-148a mimics reduced the mRNA levels of pro-inflammatory cytokines TNF-α and IL-1β.
- Histological analysis showed decreased inflammatory cell infiltration and liver cell necrosis.
- TUNEL assay indicated reduced hepatocellular apoptosis following miR-148a mimic treatment.
Conclusions:
- miR-148a plays a protective role in hepatic I/R injury.
- Inhibition of CaMKIIα by miR-148a is a key mechanism underlying its protective effect.
- miR-148a represents a potential therapeutic target for mitigating hepatic I/R injury.
