[The miR-148a alleviates hepatic ischemia/reperfusion injury in mice via targeting CaMKIIα].

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.

• Authors: Daofeng Zheng, Diao He, Xiuxian Lu, Chao Sun, Qingbo Luo, Zhongjun Wu
• Journal: Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology (Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi) Vol. 32 Issue 9 Pg. 1202-6 (Sep 2016) ISSN: 1007-8738 [Print] China
• PMID: 27609576 (Publication Type: Journal Article)

Chemical References

• MicroRNAs
• Mirn148 microRNA, mouse
• Calcium-Calmodulin-Dependent Protein Kinase Type 2
• Calcium

Topics

• Animals
• Apoptosis
• Calcium (metabolism)
• Calcium-Calmodulin-Dependent Protein Kinase Type 2 (genetics, metabolism)
• Humans
• Liver (metabolism, surgery)
• Liver Diseases (genetics, metabolism, physiopathology, surgery)
• Male
• Mice
• Mice, Inbred C57BL
• MicroRNAs (genetics, metabolism)
• Reperfusion Injury (genetics, metabolism, physiopathology)