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绵羊肺微血管内皮细胞感染蓝舌病病毒的全转录组分析。

Whole-transcriptome analyses of ovine lung microvascular endothelial cells infected with bluetongue virus.

机构信息

College of Veterinary Medicine, Southwest University, Rongchang, Chongqing, 402460, China.

Chongqing Veterinary Science Engineering Research Center, Rongchang, Chongqing, 402460, China.

出版信息

Vet Res. 2024 Sep 27;55(1):122. doi: 10.1186/s13567-024-01372-0.

Abstract

Bluetongue virus (BTV) infection induces profound and intricate changes in the transcriptional profile of the host to facilitate its survival and replication. However, there have been no whole-transcriptome studies on ovine lung microvascular endothelial cells (OLMECs) infected with BTV. In this study, we comprehensively analysed the whole-transcriptome sequences of BTV-1 serotype-infected and mock-infected OLMECs and subsequently performed bioinformatics differential analysis. Our analysis revealed 1215 differentially expressed mRNA transcripts, 82 differentially expressed long noncoding RNAs (lncRNAs) transcripts, 63 differentially expressed microRNAs (miRNAs) transcripts, and 42 differentially expressed circular RNAs (circRNAs) transcripts. Annotation from Gene Ontology, enrichment from the Kyoto Encyclopedia of Genes and Genomes, and construction of endogenous competing RNA network analysis revealed that the differentially expressed RNAs primarily participated in viral sensing and signal transduction pathways, antiviral and immune responses, inflammation, and extracellular matrix (ECM)-related pathways. Furthermore, protein‒protein interaction network analysis revealed that BTV may regulate the conformation of ECM receptor proteins and change their biological activity through a series of complex mechanisms. Finally, on the basis of real-time fluorescence quantitative polymerase chain reaction results, the expression trends of the differentially expressed RNA were consistent with the whole-transcriptome sequencing data, such as downregulation of the expression of COL4A1, ITGA8, ITGB5, and TNC and upregulation of the expression of CXCL10, RNASEL, IRF3, IRF7, and IFIHI. This study provides a novel perspective for further investigations of the mechanism of the ECM in the BTV-host interactome and the pathogenesis of lung microvascular endothelial cells.

摘要

蓝舌病毒(BTV)感染诱导宿主转录谱发生深刻而复杂的变化,以促进其存活和复制。然而,目前还没有关于 BTV 感染绵羊肺微血管内皮细胞(OLMEC)的全转录组研究。在本研究中,我们全面分析了 BTV-1 血清型感染和模拟感染的 OLMEC 的全转录组序列,随后进行了生物信息学差异分析。我们的分析揭示了 1215 个差异表达的 mRNA 转录本、82 个差异表达的长非编码 RNA(lncRNA)转录本、63 个差异表达的 microRNA(miRNA)转录本和 42 个差异表达的环状 RNA(circRNA)转录本。基因本体注释、京都基因与基因组百科全书富集以及内源性竞争 RNA 网络分析构建揭示,差异表达的 RNA 主要参与病毒感应和信号转导途径、抗病毒和免疫反应、炎症和细胞外基质(ECM)相关途径。此外,蛋白质相互作用网络分析表明,BTV 可能通过一系列复杂的机制调节 ECM 受体蛋白的构象并改变其生物学活性。最后,基于实时荧光定量聚合酶链反应结果,差异表达 RNA 的表达趋势与全转录组测序数据一致,例如 COL4A1、ITGA8、ITGB5 和 TNC 的表达下调和 CXCL10、RNASEL、IRF3、IRF7 和 IFIHI 的表达上调。本研究为进一步研究 ECM 在 BTV-宿主互作网络中的作用机制和肺微血管内皮细胞发病机制提供了新视角。

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