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Identification and characterization of N6-methyladenosine circular RNAs in the spinal cord of morphine-tolerant rats
Morphine tolerance (MT) is a tricky problem, the mechanism of it is currently unknown. Circular RNAs (circRNAs) serve significant functions in the biological processes (BPs) of the central nervous system. N6-methyladenosine (m 6 A), as a key post-transcriptional modification of RNA, can regulate the...
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Published in: | Frontiers in neuroscience 2022-08, Vol.16, p.967768-967768 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Morphine tolerance (MT) is a tricky problem, the mechanism of it is currently unknown. Circular RNAs (circRNAs) serve significant functions in the biological processes (BPs) of the central nervous system. N6-methyladenosine (m
6
A), as a key post-transcriptional modification of RNA, can regulate the metabolism and functions of circRNAs. Here we explore the patterns of m
6
A-methylation of circRNAs in the spinal cord of morphine-tolerant rats. In brief, we constructed a morphine-tolerant rat model, performed m
6
A epitranscriptomic microarray using RNA samples collected from the spinal cords of morphine-tolerant rats and normal saline rats, and implemented the bioinformatics analysis. In the spinal cord of morphine-tolerant rats, 120 circRNAs with different m
6
A modifications were identified, 54 of which were hypermethylated and 66 of which were hypomethylated. Functional analysis of these m
6
A circRNAs found some important pathways involved in the pathogenesis of MT, such as the calcium signaling pathway. In the m
6
A circRNA-miRNA networks, several critical miRNAs that participated in the occurrence and development of MT were discovered to bind to these m
6
A circRNAs, such as miR-873a-5p, miR-103-1-5p, miR-107-5p. M
6
A modification of circRNAs may be involved in the pathogenesis of MT. These findings may lead to new insights into the epigenetic etiology and pathology of MT. |
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ISSN: | 1662-453X 1662-4548 1662-453X |
DOI: | 10.3389/fnins.2022.967768 |