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Protective effects of miRNA-589 on cerebral ischemia-reperfusion injury
G P Ma1, B Z Yang2, Y S Zhang1
1Department of Neurology, The First Hospital of Tianshui, Tianshui, China.
Abstract:
To uncover the potential influence of microRNA-589 (miRNA-589) on cerebral ischemia-reperfusion injury (IRI) and the underlying mechanism, BV2 cells were stimulated by lipopolysaccharide (LPS) or conditioned medium (CM) of primary cortical neurons undergoing oxygen-glucose deprivation (OGD). Regulatory effects of miRNA-589 on the release of inflammatory factors in BV2 cells induced with LPS or CM of primary cortical neurons undergoing OGD were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). The interaction between miRNA-589 and TRAF6 was finally assessed by dual-luciferase reporter gene assay. MiRNA-589 was downregulated in BV2 cells induced with LPS or CM of primary cortical neurons undergoing OGD. Overexpression of miRNA-589 reduced the release of inflammatory factors in LPS or CM-induced BV2 cells. TRAF6 was verified to be the downstream gene of miRNA-589, and its level was negatively regulated by miRNA-589. MiRNA-589 is downregulated following cerebral IRI and alleviates inflammatory response through negatively regulating TRAF6.
Insights
MicroRNA-589 (miRNA-589) is downregulated in cerebral ischemia-reperfusion injury (IRI). Upregulating miRNA-589 alleviates inflammation by negatively regulating TRAF6, offering a potential therapeutic target.
Area of Science:
- Neuroscience
- Molecular Biology
- Immunology
Background:
- Cerebral ischemia-reperfusion injury (IRI) involves significant inflammatory responses.
- MicroRNAs (miRNAs) play crucial roles in regulating cellular processes, including inflammation.
Purpose of the Study:
- To investigate the role of microRNA-589 (miRNA-589) in cerebral IRI.
- To elucidate the underlying molecular mechanism of miRNA-589's influence on inflammation.
Main Methods:
- Utilized BV2 cells stimulated with lipopolysaccharide (LPS) or conditioned medium (CM) from oxygen-glucose deprived (OGD) neurons.
- Assessed inflammatory factor release using quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA).
- Determined the interaction between miRNA-589 and TRAF6 via dual-luciferase reporter gene assay.
Main Results:
- miRNA-589 expression was found to be downregulated in response to LPS or OGD-induced CM.
- Overexpression of miRNA-589 significantly reduced the release of inflammatory factors.
- TRAF6 was identified as a direct downstream target of miRNA-589, with its expression negatively regulated by miRNA-589.
Conclusions:
- miRNA-589 is downregulated in cerebral IRI.
- miRNA-589 exerts a protective effect by alleviating inflammatory responses.
- The anti-inflammatory mechanism involves the negative regulation of TRAF6 by miRNA-589.
