长链非编码RNA 1810026B05Rik通过NF-κB通路激活介导脑缺血/再灌注诱导的神经元损伤

IF 4.9 2区 生物学
Hao Zhang, Meng Li, Jiayu Yao, Xuan Jiang, Junxiao Feng, Xingjuan Shi, Xiaoou Sun
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引用次数: 0

摘要

脑缺血/再灌注(I/R)损伤仍然是成人神经系统疾病的重要因素,主要是由于神经炎症和细胞凋亡加剧。这些过程通过释放各种促炎细胞因子和促凋亡介质放大脑损伤。尽管长链非编码rna (lncRNAs)越来越多地被认为参与调节多种生物通路,但它们在脑I/R损伤中的确切作用尚未完全阐明。在目前的研究中,利用大鼠局灶性脑I/R模型进行转录组学分析,鉴定出lncRNA- 1810026b05rik -也称为chaserr -是一种对缺血条件有反应的新型lncRNA。该lncRNA在大脑中动脉闭塞后再灌注(MCAO/R)的小鼠脑组织中,以及在缺氧-葡萄糖剥夺和随后的再氧合(OGD/R)的大鼠皮层原代神经元中表达升高。结果提示,lncRNA-1810026B05RiK通过物理结合NF-κB抑制剂α (i -κB α)并促进其磷酸化,介导核因子-κB (NF-κB)信号通路的激活,从而导致脑缺血/再灌注时神经炎症和神经元凋亡。此外,lncRNA-1810026B05Rik下调在OGD/R和MCAO/R病理过程中作为NF-κB抑制剂,提示lncRNA-1810026B05Rik下调对脑I/R损伤具有保护作用。综上所述,lncRNA-1810026B05Rik已被确定为通过激活NF-κB信号级联激活神经元凋亡和炎症的关键调节因子。这一发现揭示了1810026B05Rik在缺血性卒中分子机制中的作用,为疾病病理学提供了有价值的见解。此外,它的参与突出了它作为一种新的治疗靶点的潜力,为卒中患者的创新治疗策略铺平了道路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Long Non-Coding RNA 1810026B05Rik Mediates Cerebral Ischemia/Reperfusion-Induced Neuronal Injury Through NF-κB Pathway Activation.

Cerebral ischemia/reperfusion (I/R) injury remains a significant contributor to adult neurological morbidity, primarily due to exacerbated neuroinflammation and cell apoptosis. These processes amplify brain damage through the release of various pro-inflammatory cytokines and pro-apoptotic mediators. Although long non-coding RNAs (lncRNAs) are increasingly recognized for their involvement in regulating diverse biological pathways, their precise role in cerebral I/R injury has not been fully elucidated. In the current study, transcriptomic profiling was conducted using a rat model of focal cerebral I/R, leading to the identification of lncRNA-1810026B05Rik-also referred to as CHASERR-as a novel lncRNA responsive to ischemic conditions. The elevated expression of this lncRNA was observed in mouse brain tissues subjected to middle cerebral artery occlusion followed by reperfusion (MCAO/R), as well as in primary cortical neurons derived from rats exposed to oxygen-glucose deprivation and subsequent reoxygenation (OGD/R). The results suggested that lncRNA-1810026B05RiK mediates the activation of the nuclear factor-kappaB (NF-κB) signaling pathway by physically binding to NF-kappa-B inhibitor alpha (IκBα) and promoting its phosphorylation, thus leading to neuroinflammation and neuronal apoptosis during cerebral ischemia/reperfusion. In addition, lncRNA-1810026B05Rik knockdown acts as an NF-κB inhibitor in the OGD/R and MCAO/R pathological processes, suggesting that lncRNA-1810026B05Rik downregulation exerts a protective effect on cerebral I/R injury. In summary, the lncRNA-1810026B05Rik has been identified as a critical regulator of neuronal apoptosis and inflammation through the activation of the NF-κB signaling cascade. This discovery uncovers a previously unrecognized role of 1810026B05Rik in the molecular mechanisms underlying ischemic stroke, offering valuable insights into disease pathology. Moreover, its involvement highlights its potential as a novel therapeutic target, paving the way for innovative treatment strategies for stroke patients.

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来源期刊
自引率
10.70%
发文量
13472
审稿时长
1.7 months
期刊介绍: The International Journal of Molecular Sciences (ISSN 1422-0067) provides an advanced forum for chemistry, molecular physics (chemical physics and physical chemistry) and molecular biology. It publishes research articles, reviews, communications and short notes. Our aim is to encourage scientists to publish their theoretical and experimental results in as much detail as possible. Therefore, there is no restriction on the length of the papers or the number of electronics supplementary files. For articles with computational results, the full experimental details must be provided so that the results can be reproduced. Electronic files regarding the full details of the calculation and experimental procedure, if unable to be published in a normal way, can be deposited as supplementary material (including animated pictures, videos, interactive Excel sheets, software executables and others).
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