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Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
Published on: August 25, 2017
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Long non-coding RNA Snhg16 Lessens Ozone Curative Effect on Chronic Constriction Injury mice via microRNA-719/SCN1A
Jianning Yue1, Qi Wang2, Wenxing Zhao2
1Department of Pain Management, Xuanwu Hospital, Capital Medical University, 45, Changchun Street, Xicheng District, Beijing, 100053, China. yuejn@163.com.
Molecular Biotechnology
|August 26, 2023
Summary
Long non-coding RNA Snhg16 promotes neuropathic pain (NP) by interacting with miR-719 to upregulate SCN1A. This axis impacts ozone therapy effectiveness for NP in mice.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Neuropathic pain (NP) is a debilitating condition often linked to neuroinflammation.
- Ozone therapy shows potential for NP treatment, but its mechanism requires elucidation.
- Long non-coding RNAs (lncRNAs) play critical roles in various biological processes, including pain.
Purpose of the Study:
- To investigate the role of lncRNA Snhg16 in neuropathic pain (NP) and its interaction with ozone therapy.
- To elucidate the molecular mechanism of Snhg16 in NP development.
- To explore the Snhg16/miR-719/SCN1A axis in the context of NP and ozone treatment.
Main Methods:
- Mouse model of chronic constriction injury (CCI) for NP induction.
- Behavioral tests (PWT, PLN, PWL) to assess pain responses.
- ELISA and qRT-PCR for neuroinflammation and gene expression analysis.
- Bioinformatics, dual-luciferase reporter assay, and RNA pull-down for mechanism validation.
Main Results:
- Snhg16 expression was elevated in CCI mice, exacerbating NP and hindering ozone therapy efficacy.
- Snhg16 acted as a molecular sponge for miR-719, and SCN1A was identified as a target of miR-719.
- Inhibition of miR-719 reversed Snhg16-induced pain behaviors and neuroinflammation.
- SCN1A upregulation partially counteracted the protective effects of miR-719.
Conclusions:
- lncRNA Snhg16 promotes NP progression in CCI mice via the Snhg16/miR-719/SCN1A pathway.
- This molecular axis negatively influences the therapeutic effects of ozone therapy for NP.
- Targeting the Snhg16/miR-719/SCN1A axis offers a potential strategy for NP treatment.
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