Abstract
Background: N6-methyladenosine (m6A) is the most prevalent modification in mRNAs but its role in lumbosacral nerve root avulsion (LSRA) remains elusive. Materials&methods:Mettl3 expression and global m6A level were detected by qPCR, western blot and immunostaining. Altered m6A-tagged transcript profiles were revealed by methylated RNA immunoprecipitation and RNA sequencing. Results:Mettl3 and global m6A level were upregulated in spinal cord tissues of LSRA rats. In all, 1087 m6A peaks were differentially modified by m6A, of which 654 were upregulated and 433 downregulated. Biological functions of these transcripts and the hypermethylated or hypomethylated transcripts were also identified. Conclusion: Our findings revealed a profound function of m6A modification in LSRA, which provides new insights into its pathogenesis.
Supplementary data
To view the supplementary data that accompany this paper please visit the journal website at: www.tandfonline.com/doi/suppl/10.2217/epi-2022-0127
Author contributions
Z Zhou and L Zhu designed the research. Z Zhou wrote the manuscript and conducted the experiments. Z Zhou and L Zhu analyzed the data. L Zhu revised the manuscript and was responsible for supervision of the study.
Financial&competing interests disclosure
This study was funded by the special project for clinical research of Shanghai Health Commission (grant no. 20194Y0451). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.
Ethical conduct of research
The authors state that they have obtained appropriate institutional review board approval or have followed the principles outlined in the Declaration of Helsinki for all human or animal experimental investigations.
Data sharing statement
All data for this study can be found in the Supplementary Data. Further information and requests for resources and reagents should be directed to and will be fulfilled by the corresponding author.