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24. SENP5 deteriorates traumatic brain injury via SUMO2-dependent suppression of E2F1 SUMOylation

Author

Ding Yanfu, Chen Feifei, Yang Weitao, Fu Xiaobin, and Xie Yuanyuan

Subjects
traumatic brain injury, SENP5, E2F1, SUMOylation, p53 signaling pathway, Biochemistry, QD415-436, Genetics, QH426-470
Abstract

Traumatic brain injury (TBI) represents a main public health concern during the past decade, attracting considerable interest because of its rising prevalence, wide-ranging risk factors and lifelong familial and societal influence. SUMO2 can conjugate to substrates upon various cellular stresses. Nevertheless, whether and how SUMO2-specific proteases partake in TBI is less understood. The aim of this study is to dissect the effects of SUMO-specific peptidase 5 (SENP5) on accentuating TBI in rats in an effort to unveil its underlying mechanism. SENP5 is overexpressed in hippocampal tissues of TBI rats, and inhibition of SENP5 reduces neurological function scores, decreases brain water content, inhibits apoptosis in hippocampal tissues, and attenuates brain injury caused in rats. Moreover, SENP5 inhibits the SUMOylation level of E2F transcription factor 1 (E2F1) and increases the protein expression of E2F1. Silencing of E2F1 blocks the p53 signaling pathway. Overexpression of E2F1 partially reverses the protective effect of sh-SENP5 on TBI in rats. These findings reveal an essential role of SENP5 and the SUMOylation status of E2F1 in the TBI development.

Published
2023
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33. Novel rare genetic variants of familial and sporadic pulmonary atresia identified by whole-exome sequencing

Author

Xing Junyue, Wang Hongdan, Xie Yuanyuan, Fan Taibing, Cui Cunying, Li Yanan, Wang Shuai, Gu Weiyue, Wang Chengzeng, Tang Hao, and Liu Lin

Subjects
pulmonary atresia, whole-exome sequencing, rare variants, genetics, Biology (General), QH301-705.5
Abstract

Pulmonary atresia (PA) is a severe cyanotic congenital heart disease. Although some genetic mutations have been described to be associated with PA, the knowledge of pathogenesis is insufficient. The aim of this research was to use whole-exome sequencing (WES) to determine novel rare genetic variants in PA patients. We performed WES in 33 patients (27 patient–parent trios and 6 single probands) and 300 healthy control individuals. By applying an enhanced analytical framework to incorporate de novo and case–control rare variation, we identified 176 risk genes (100 de novo variants and 87 rare variants). Protein‒protein interaction (PPI) analysis and Genotype-Tissue Expression analysis revealed that 35 putative candidate genes had PPIs with known PA genes with high expression in the human heart. Expression quantitative trait loci analysis revealed that 27 genes that were identified as novel PA genes that could be affected by the surrounding single nucleotide polymorphism were screened. Furthermore, we screened rare damaging variants with a threshold of minor allele frequency at 0.5% in the ExAC_EAS and GnomAD_exome_EAS databases, and the deleteriousness was predicted by bioinformatics tools. For the first time, 18 rare variants in 11 new candidate genes have been identified that may play a role in the pathogenesis of PA. Our research provides new insights into the pathogenesis of PA and helps to identify the critical genes for PA.

Published
2023
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