Qingbin Wu1, Xiaochen Yuan1, Ruiqin Han2, Honggang Zhang1, Ruijuan Xiu1. 1. Key Laboratory for Microcirculation, Ministry of Health; Institute of Microcirculation, Chinese Academy Medical Sciences & Pecking Union Medical College, Beijing, 100005, PR China. 2. Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, 100005, PR China.
Abstract
Aim: Pericytes maintain homeostatic functions in the blood-brain barrier. N6-methyladenosine (m6A) is critical for various biological processes, but the role of mRNA m6A methylation in hypertension has not been fully elucidated. Methods: The m6A methylation levels of Wistar Kyoto rat pericytes and spontaneously hypertensive rat pericytes were detected via m6A high-throughput sequencing. Results: The m6A methylations were more enriched in the coding sequence region, 3'UTR and 5'UTR of mRNAs, with the m6A motifs being relatively conserved across the different conditions investigated. The average m6A abundance of spontaneously hypertensive rat pericytes exhibited global reductions in the pericytes. Conclusion: This study revealed the m6A landscapes and identified an epitranscriptomic mechanism during the development of mammalian hypertension.
Aim: Pericytes maintain homeostatic functions in the blood-brain barrier. N6-methyladenosine (m6A) is critical for various biological processes, but the role of mRNA m6A methylation in hypertension has not been fully elucidated. Methods: The m6A methylation levels of Wistar Kyoto rat pericytes and spontaneously hypertensiverat pericytes were detected via m6A high-throughput sequencing. Results: The m6A methylations were more enriched in the coding sequence region, 3'UTR and 5'UTR of mRNAs, with the m6A motifs being relatively conserved across the different conditions investigated. The average m6A abundance of spontaneously hypertensiverat pericytes exhibited global reductions in the pericytes. Conclusion: This study revealed the m6A landscapes and identified an epitranscriptomic mechanism during the development of mammalianhypertension.