Lu Tingting, Song Xinghui, Zhao Li, Ma Xia
Am J Vet Res. 2024 Oct 28;85(12). doi: 10.2460/ajvr.24.06.0164. Print 2024 Dec 1.
This study aims to identify and characterize differentially expressed genes (DEGs) associated with porcine parvovirus (PPV)-induced cell death in porcine kidney-15 (PK-15) cells. By analyzing the biological processes enriched by these DEGs and exploring their interaction networks, we aim to gain a deeper understanding of the molecular mechanisms underlying PPV-mediated cell death.
After infecting cultured PK-15 cells with PPV for 24 and 48 hours, cell viability and cysteine-requiring aspartate protease-3 (caspase-3) activity were assessed using an enzyme marker. Apoptosis was observed using fluorescence microscopy. The genome-wide gene expression levels were analyzed through RNA sequencing. The functional enrichment of DEGs was analyzed using the Kyoto Encyclopedia of Genes and Genomes database, and the protein-protein interaction network was generated using the Search Tool for the Retrieval of Interacting Genes/Proteins database.
Porcine parvovirus inhibits cell viability, boosts caspase-3 activity, and enhances cell death at 24 and 48 hours postinfection (HPI). Porcine parvovirus-infected cells showed 547 DEGs at 24 HPI and 1,765 at 48 HPI. Different forms of cell death were enriched in 149 genes that were upregulated at both 24 and 48 HPI. More DEGs associated with cell death were involved at 48 than at 24 HPI. These DEGs are involved in multiple signaling pathways and interact within a complex protein network.
Porcine parvovirus infection of PK-15 cells induces multiple cell death-related DEGs and signaling pathways.
Our study presents a promising approach to investigating the mechanism of PPV infection, with a particular focus on the induction of cell death.
本研究旨在鉴定和表征与猪细小病毒（PPV）诱导猪肾-15（PK-15）细胞死亡相关的差异表达基因（DEG）。通过分析这些DEG富集的生物学过程并探索其相互作用网络，我们旨在更深入地了解PPV介导的细胞死亡的分子机制。
用PPV感染培养的PK-15细胞24小时和48小时后，使用酶标记物评估细胞活力和半胱氨酸天冬氨酸蛋白酶-3（caspase-3）活性。用荧光显微镜观察细胞凋亡。通过RNA测序分析全基因组基因表达水平。使用京都基因与基因组百科全书数据库分析DEG的功能富集，并使用检索相互作用基因/蛋白质的搜索工具数据库生成蛋白质-蛋白质相互作用网络。
猪细小病毒在感染后24小时和48小时抑制细胞活力，提高caspase-3活性，并增强细胞死亡。猪细小病毒感染的细胞在感染后24小时显示547个DEG，在48小时显示1,765个DEG。不同形式的细胞死亡在感染后24小时和48小时均上调的149个基因中富集。与细胞死亡相关的DEG在48小时比在24小时更多。这些DEG参与多个信号通路并在复杂的蛋白质网络中相互作用。
PK-15细胞感染猪细小病毒可诱导多个与细胞死亡相关的DEG和信号通路。
我们的研究提出了一种有前景的方法来研究PPV感染的机制，特别关注细胞死亡的诱导。
