Abstract
Messager RNA (mRNA) can be modified in a variety of ways, among which the modification of N6-methyladenosine (m6A) is one of the most common ones. Recent studies have found that the m6A modification in mRNA could functionally regulate the splicing, localization, translation, and stability of mRNA, which might be closely related to multiple diseases. However, the roles of m6A modification in traumatic optic neuropathy (TON) are unknown. Herein, we detected the expression of m6A-related genes via quantitative real-time PCR (qRT-PCR) and performed methylated RNA immunoprecipitation sequencing (MeRIP-seq) as well as RNA-sequencing to analyze the alteration profiles of m6A modification after TON. The results showed that the expression of m6A-related genes (METTL3, WTAP, FTO, and ALKBH5) were all upregulated after TON. In all, 2,810 m6A peaks were differentially upregulated and 689 m6A peaks were downregulated. In addition, the hypermethylated and hypomethylated profiles of mRNA transcripts were also identified. To sum up, our study revealed the differentially expressed m6A modification in the early stage of TON, which may provide novel insights into the mechanism and treatment of TON.
Highlights
Traumatic optic neuropathy (TON) refers to a common complication of traumatic brain injury (TBI), and the incidence of traumatic optic neuropathy (TON) ranges from 1.5 to 4% (Guy et al, 2014)
The expression levels of m6A-related genes FTO, ALKBH5, METTL3 and WTAP in the retina of injured and sham-operated rats were analyzed by using quantitative real-time PCR (qRT-PCR)
According to the Gene ontology (GO) analysis, the upregulated peaks in the TON retina were significantly associated with protein binding, nervous system development, and intracellular
Summary
Traumatic optic neuropathy (TON) refers to a common complication of traumatic brain injury (TBI), and the incidence of TON ranges from 1.5 to 4% (Guy et al, 2014). A large number of nucleotide modifications have been found to be abundant in eukaryotic mRNAs, such as m6A, 5-methylcytosine (m5C), and N1-methyladenosine (m1A; Maity and Das, 2016). The development of methylated RNA immunoprecipitation sequencing (MeRIP-seq) and other technologies have increased our understanding of the role of m6A modifications in mRNAs. Regulated by methyltransferases (METTL3, METTL14, WTAP, etc.) and demethylases (FTO, ALKBH5, etc.), m6A modification is capable of participating in various fundamental biological mechanisms, for example, the regulation of gene expression, self-renewal of neural stem cells, the formation of metabolic diseases, the maintenance of biological circadian rhythms, and the development of cancers (Fischer et al, 2009; Fustin et al, 2013; Zhou et al, 2015, 2018; Maity and Das, 2016; Hsu et al, 2017). This study revealed some potential roles of m6A-modified transcripts in TON
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