Yiqin Wang1, Jian Mao2, Xin Wang3, Yong Lin2, Guoqiang Hou2, Jun Zhu1, Baoshu Xie2,4. 1. CNRS-LIA Hematology and Cancer, Sino-French Research Center for Life Sciences & Genomics, State Key Laboratory of Medical Genomics, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, PR China. 2. Department of Neurosurgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, PR China. 3. Department of Anesthesiology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, 160 Pujian Road, Pudong New District, Shanghai 200127, PR China. 4. Department of Neurosurgery, First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, Guangdong Province, PR China.
Abstract
Aim: To systematically profile RNA m6A modification landscape after traumatic brain injury (TBI) in mice. Materials & methods: Expression of m6A-related genes was detected by quantitative real-time PCR (qPCR). Expression and location of METTL3, a key component of m6A methyltransferase complex, were determined by immunostaining. Genome-wide profiling of m6A-tagged transcripts was conducted by m6A-modified RNA immunoprecipitation sequencing (m6A-RIP-seq) and RNA sequencing (RNA-seq). Results: METTL3 was downregulated after TBI. In total, 922 m6A peaks were differentially expressed as determined by m6A-RIP-seq, with 370 upregulated and 552 downregulated. In addition, we identified differentially expressed hypomethylated and hypermethylated mRNA transcripts. Conclusion: Our data provided novel information regarding m6A modification changes in the early period of TBI, which might be promising therapy targets.
Aim: To systematically profile RNA m6A modification landscape after traumatic brain injury (TBI) in mice. Materials & methods: Expression of m6A-related genes was detected by quantitative real-time PCR (qPCR). Expression and location of METTL3, a key component of m6A methyltransferase complex, were determined by immunostaining. Genome-wide profiling of m6A-tagged transcripts was conducted by m6A-modified RNA immunoprecipitation sequencing (m6A-RIP-seq) and RNA sequencing (RNA-seq). Results:METTL3 was downregulated after TBI. In total, 922 m6A peaks were differentially expressed as determined by m6A-RIP-seq, with 370 upregulated and 552 downregulated. In addition, we identified differentially expressed hypomethylated and hypermethylated mRNA transcripts. Conclusion: Our data provided novel information regarding m6A modification changes in the early period of TBI, which might be promising therapy targets.