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凋亡拮抗转录因子参与大鼠创伤后癫痫的发病机制。

Apoptosis-antagonizing transcription factor is involved in rat post-traumatic epilepsy pathogenesis.

作者信息

Wang Wei, Ma Yu-Min, Jiang Zheng-Lin, Gao Zhi-Wei, Chen Wei-Guan

机构信息

Department of Neurology, Affiliated Hospital of Nantong University, Nantong, Jiangsu 226001, P.R. China.

Department of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China.

出版信息

Exp Ther Med. 2021 Apr;21(4):290. doi: 10.3892/etm.2021.9721. Epub 2021 Jan 27.

DOI:10.3892/etm.2021.9721
PMID:33717233
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7885077/
Abstract

The present study aimed to explore the pathogenesis behind post-traumatic epilepsy (PTE). In the present study, a chloride ferric injection-induced rat PTE model was established. The expression levels of apoptosis-antagonizing transcription factor (AATF), cleaved caspase-3, p53, Bcl-2 and Bax were measured by western blotting or immunofluorescence staining (IF). The expression of AATF was downregulated by microinjection of lentiviral-mediated short-hairpin RNA. Compared with control and sham groups, at day 5 after PTE, neuron apoptosis was significantly increased and the expression levels of AATF, p53, cleaved caspase-3 and Bax were significantly upregulated. In addition, IF revealed co-localization of AATF and cleaved caspase-3 in the cortex. Additionally, AATF was expressed mainly in neurons and astrocytes. Following AATF inhibition, the expression levels of p53 and cleaved caspase-3 were significantly reduced as compared with the control group. Taken together, these findings suggested that following PTE, AATF is involved in neuronal apoptosis and may serve as a potential target for its alleviation.

摘要

本研究旨在探讨创伤后癫痫（PTE）背后的发病机制。在本研究中，建立了氯化铁注射诱导的大鼠PTE模型。通过蛋白质免疫印迹法或免疫荧光染色（IF）检测凋亡拮抗转录因子（AATF）、裂解的半胱天冬酶-3、p53、Bcl-2和Bax的表达水平。通过显微注射慢病毒介导的短发夹RNA下调AATF的表达。与对照组和假手术组相比，PTE后第5天，神经元凋亡显著增加，AATF、p53、裂解的半胱天冬酶-3和Bax的表达水平显著上调。此外，IF显示AATF和裂解的半胱天冬酶-3在皮质中共定位。此外，AATF主要在神经元和星形胶质细胞中表达。抑制AATF后，与对照组相比，p53和裂解的半胱天冬酶-3的表达水平显著降低。综上所述，这些发现表明，PTE后，AATF参与神经元凋亡，可能是缓解PTE的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a9/7885077/8ee00a8d4e22/etm-21-04-09721-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a9/7885077/b4e165ae8290/etm-21-04-09721-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a9/7885077/a94627f0ffb8/etm-21-04-09721-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a9/7885077/8a0bd73296a9/etm-21-04-09721-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a9/7885077/2a73092a7e0f/etm-21-04-09721-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a9/7885077/8ee00a8d4e22/etm-21-04-09721-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a9/7885077/b4e165ae8290/etm-21-04-09721-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a9/7885077/a94627f0ffb8/etm-21-04-09721-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a9/7885077/8a0bd73296a9/etm-21-04-09721-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a9/7885077/2a73092a7e0f/etm-21-04-09721-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a9/7885077/8ee00a8d4e22/etm-21-04-09721-g04.jpg

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