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TRPM4 Drives Cerebral Edema by Switching to Alternative Splicing Isoform After Experimental Traumatic Brain Injury

创伤性脑损伤 选择性拼接 医学 水肿 脑水肿 基因亚型 神经科学 生物信息学 病理 生物 内科学 精神科 基因 遗传学
作者
Lihan Zhang,Chaojie Li,Yijing He,Chenghao Kuang,Xiancheng Qiu,Lianzhi Gu,Jinpeng Wu,Jinwei Pang,Lifang Zhang,Bingqing Xie,Jianhua Peng,Shigang Yin,Yong Jiang
出处
期刊:Journal of Neurotrauma [Mary Ann Liebert]
卷期号:40 (15-16): 1779-1795
标识
DOI:10.1089/neu.2022.0503
摘要

Traumatic brain injury (TBI) affects persons of all ages and is recognized as a major cause of death and disability worldwide; it also brings heavy life burden to patients and their families. The treatment of those with secondary injury after TBI is still scarce, however. Alternative splicing (AS) is a crucial post-transcriptional regulatory mechanism associated with various physiological processes, while the contribution of AS in treatment after TBI is poorly illuminated. In this study, we performed and analyzed the transcriptome and proteome datasets of brain tissue at multiple time points in a controlled cortical impact (CCI) mouse model. We found that AS, as an independent change against the transcriptional level, is a novel mechanism linked to cerebral edema after TBI. Bioinformatics analysis further indicated that the transformation of splicing isoforms after TBI was related to cerebral edema. Accordingly, we found that the fourth exon of transient receptor potential channel melastatin 4 (Trpm4) abrogated skipping at 72 h after TBI, resulting in a frameshift of the encoded amino acid and an increase in the proportion of spliced isoforms. Using magnetic resonance imaging (MRI), we have shown the numbers of 3nEx isoforms of Trpm4 may be positively correlated with volume of cerebral edema. Thus alternative splicing of Trpm4 becomes a noteworthy mechanism of potential influence on edema. In summary, alternative splicing of Trpm4 may drive cerebral edema after TBI. Trpm4 is a potential therapeutic targeting cerebral edema in patients with TBI.
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