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Investigating the Mechanism by Which RMRP Regulates Diabetic Peripheral Neuropathy via the miR-3142
Mimi Wang1, Tenghui Fu2, Jinfeng Yang3
1Department of Endocrinology, Xuzhou Tongshan District Traditional Chinese Medicine Hospital, Xuzhou, China.
Abstract:
This study aims to investigate the role of long noncoding RNA RMRP in diabetic peripheral neuropathy (DPN) and its potential mechanisms. We used high glucose (HG) treatment on Schwann cells (SCs) and established a DPN rat model to study the role of RMRP in DPN. RT-qPCR was employed to assess the levels of RMRP and miR-3142. The targeting relationship between RMRP and miR-3142 was verified through dual-luciferase reporter assays, RIP assays, and RNA pull-down experiments. CCK-8 assays and flow cytometry were used to evaluate cell proliferation and apoptosis. The von Frey test and thermal stimulus apparatus measured the mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) in rats. In addition, the motor nerve conduction velocity (MNCV) and sensory nerve conduction velocity (SNCV) of the rats were assessed. RMRP was abnormally expressed in both HG-treated SCs and DPN rats. Inhibition of RMRP significantly alleviated the reduction in SCs proliferation and the increase in apoptosis induced by HG, while also reducing oxidative stress and neuroinflammation levels. In DPN rats, inhibition of RMRP improved MWT and TWL and enhanced nerve conduction velocity, whereas inhibition of miR-3142 diminished the protective effects of si-RMRP. Inhibiting RMRP can relieve DPN-related oxidative stress and cell inflammation, as well as reduce pain hypersensitivity and the decline in nerve conduction velocity in rats by upregulating miR-3142.
Insights
Long noncoding RNA RMRP plays a key role in diabetic peripheral neuropathy (DPN). Inhibiting RMRP alleviates DPN symptoms and nerve damage by upregulating miR-3142.
Area of Science:
- Molecular Biology
- Neuroscience
- Endocrinology
Background:
- Diabetic peripheral neuropathy (DPN) is a common complication of diabetes.
- The role of long noncoding RNAs (lncRNAs) in DPN pathogenesis is increasingly recognized.
- Schwann cells (SCs) are crucial for peripheral nerve function and are affected in DPN.
Purpose of the Study:
- To investigate the role of lncRNA RMRP in DPN.
- To elucidate the underlying molecular mechanisms of RMRP in DPN.
- To explore the relationship between RMRP and miR-3142 in DPN.
Main Methods:
- Established a high glucose (HG)-treated SCs model and a DPN rat model.
- Quantified RMRP and miR-3142 expression using RT-qPCR.
- Validated RMRP-miR-3142 interaction via dual-luciferase reporter, RIP, and RNA pull-down assays.
- Assessed cell proliferation and apoptosis using CCK-8 and flow cytometry.
- Evaluated DPN phenotypes in rats, including nerve conduction velocity (NCV) and behavioral tests (MWT, TWL).
Main Results:
- RMRP was upregulated in HG-treated SCs and DPN rats.
- RMRP inhibition improved SCs proliferation, reduced apoptosis, oxidative stress, and neuroinflammation.
- In DPN rats, RMRP inhibition ameliorated pain hypersensitivity and improved MWT, TWL, and NCV.
- Inhibition of miR-3142 reversed the protective effects of RMRP inhibition.
Conclusions:
- lncRNA RMRP is a critical mediator in DPN development.
- RMRP exacerbates DPN by promoting oxidative stress and neuroinflammation.
- RMRP inhibition offers a potential therapeutic strategy for DPN by upregulating miR-3142, thereby reducing pain and improving nerve function.
