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胆红素给药调节与脑缺血再灌注损伤中神经保护相关的 microRNA-mRNA 表达网络。

Biliverdin administration regulates the microRNA-mRNA expressional network associated with neuroprotection in cerebral ischemia reperfusion injury in rats.

机构信息

Department of Anesthesiology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650000, P.R. China.

Experimental Animal Center, Kunming Medical University, Kunming, Yunnan 650000, P.R. China.

出版信息

Int J Mol Med. 2019 Mar;43(3):1356-1372. doi: 10.3892/ijmm.2019.4064. Epub 2019 Jan 14.

DOI:10.3892/ijmm.2019.4064
PMID:30664169
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6365090/
Abstract

Inflammatory response has an important role in the outcome of cerebral ischemia reperfusion injury (CIR). Biliverdin (BV) administration can relieve CIR in rats, but the mechanism remains unknown. The aim of the present study was to explore the expressional network of microRNA (miRNA)‑mRNA in CIR rats following BV administration. A rat middle cerebral artery occlusion model with BV treatment was established. After neurobehavior was evaluated by neurological severity scores (NSS), miRNA and mRNA expressional profiles were analyzed by microarray technology from the cerebral cortex subjected to ischemia and BV administration. Then, bioinformatics prediction was used to screen the correlation between miRNA and mRNA, and 20 candidate miRNAs and 33 candidate mRNAs were verified by reverse transcription‑quantitative polymerase chain reaction. Furthermore, the regulation relationship between ETS proto‑oncogene 1 (Ets1) and miRNA204‑5p was examined by luciferase assay. A total of 86 miRNAs were differentially expressed in the BV group compared with the other groups. A total of 10 miRNAs and 26 candidate genes were identified as a core 'microRNA‑mRNA' regulatory network that was linked with the functional improvement of BV administration in CIR rats. Lastly, the luciferase assay results confirmed that miRNA204‑5p directly targeted Ets1. The present findings suggest that BV administration may regulate multiple miRNAs and mRNAs to improve neurobehavior in CIR rats, by influencing cell proliferation, apoptosis, maintaining ATP homeostasis, and angiogenesis.

摘要

炎症反应在脑缺血再灌注损伤 (CIR) 的结果中具有重要作用。胆红素 (BV) 给药可减轻 CIR 大鼠的损伤，但机制尚不清楚。本研究旨在探讨 BV 给药后 CIR 大鼠中 microRNA (miRNA)-mRNA 的表达网络。建立了 BV 治疗的大鼠大脑中动脉闭塞模型。通过神经严重程度评分 (NSS) 评估神经行为后，采用微阵列技术分析缺血和 BV 给药后大脑皮质中的 miRNA 和 mRNA 表达谱。然后，通过生物信息学预测筛选 miRNA 和 mRNA 之间的相关性，并通过逆转录-定量聚合酶链反应验证 20 个候选 miRNA 和 33 个候选 mRNA。此外，通过荧光素酶测定法检查 ETS 原癌基因 1 (Ets1) 和 miRNA204-5p 之间的调节关系。与其他组相比，BV 组共有 86 个 miRNA 表达差异。确定了 10 个 miRNA 和 26 个候选基因作为与 CIR 大鼠中 BV 给药功能改善相关的核心“miRNA-mRNA”调控网络。最后，荧光素酶测定结果证实 miRNA204-5p 可直接靶向 Ets1。本研究结果表明，BV 给药可能通过影响细胞增殖、凋亡、维持 ATP 稳态和血管生成来调节多种 miRNA 和 mRNAs，从而改善 CIR 大鼠的神经行为。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8101/6365090/2d0feb99eea8/IJMM-43-03-1356-g08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8101/6365090/3a83e48dee4f/IJMM-43-03-1356-g00.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8101/6365090/84fc8265e58a/IJMM-43-03-1356-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8101/6365090/58a442503594/IJMM-43-03-1356-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8101/6365090/835b6ebd3592/IJMM-43-03-1356-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8101/6365090/5577d537c5b1/IJMM-43-03-1356-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8101/6365090/f874fd001ed8/IJMM-43-03-1356-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8101/6365090/2d0feb99eea8/IJMM-43-03-1356-g08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8101/6365090/3a83e48dee4f/IJMM-43-03-1356-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8101/6365090/a675cd6815c6/IJMM-43-03-1356-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8101/6365090/84fc8265e58a/IJMM-43-03-1356-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8101/6365090/58a442503594/IJMM-43-03-1356-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8101/6365090/835b6ebd3592/IJMM-43-03-1356-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8101/6365090/5577d537c5b1/IJMM-43-03-1356-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8101/6365090/f874fd001ed8/IJMM-43-03-1356-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8101/6365090/2d0feb99eea8/IJMM-43-03-1356-g08.jpg

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