Overview of long non-coding RNA and mRNA expression in response to methamphetamine treatment in vitro
Kun Xiong1, Lingling Long2, Xudong Zhang3
1Department of Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, Hunan 410013, China.
Abstract:
Long non-coding RNAs (lncRNAs) display multiple functions including regulation of neuronal injury. However, their impact in methamphetamine (METH)-induced neurotoxicity has rarely been reported. Here, using microarray analysis, we investigated the expression profiling of lncRNAs and mRNAs in primary cultured prefrontal cortical neurons after METH treatment. We observed a difference in lncRNA and mRNA expression between the experimental and sham control groups. Using bioinformatics, we analyzed the highest enriched gene ontology (GO) terms of biological process, cellular component, and molecular function, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and pathway network analysis. Furthermore, an lncRNA-mRNA co-expression sub-network for aberrantly expressed terms revealed possible interactions of lncRNA NR_110713 and NR_027943 with their related genes. Afterwards, three lncRNAs (NR_110713, NR_027943, GAS5) and two mRNAs (Ddit3, Casp12) were targeted to validate the microarray data by qRT-PCR. This presented an overview of lncRNA and mRNA expression profiling and indicated that lncRNA might participate in METH-induced neuronal apoptosis by regulating the coding genes of neurons.
Insights
Long non-coding RNAs (lncRNAs) are implicated in neuronal injury. This study reveals lncRNA dysregulation in methamphetamine-induced neurotoxicity, suggesting their role in neuronal apoptosis.
Area of Science:
- Neuroscience
- Molecular Biology
- Genomics
Background:
- Long non-coding RNAs (lncRNAs) regulate neuronal functions, but their role in methamphetamine (METH)-induced neurotoxicity is understudied.
- Methamphetamine abuse leads to significant neurotoxicity, impacting neuronal health and function.
Purpose of the Study:
- To investigate the expression profiles of lncRNAs and messenger RNAs (mRNAs) in primary cortical neurons following METH treatment.
- To identify potential lncRNA-mRNA interactions involved in METH-induced neurotoxicity.
Main Methods:
- Microarray analysis was employed to profile lncRNA and mRNA expression in cultured neurons exposed to METH.
- Bioinformatic analyses, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, were performed.
- Quantitative real-time PCR (qRT-PCR) was used to validate the expression of selected lncRNAs and mRNAs.
Main Results:
- Significant differences in lncRNA and mRNA expression were observed between METH-treated and control groups.
- Bioinformatics identified enriched GO terms and KEGG pathways associated with METH exposure.
- A co-expression sub-network highlighted potential interactions between lncRNAs (NR_110713, NR_027943) and mRNAs.
Conclusions:
- lncRNAs exhibit altered expression patterns in response to METH-induced neurotoxicity.
- lncRNAs may play a role in METH-induced neuronal apoptosis by modulating the expression of protein-coding genes.
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