Upregulation of FABP7 inhibits acute kidney injury-induced TCMK-1 cell apoptosis via activating the PPAR gamma signalling pathway,Molecular Omics

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Upregulation of FABP7 inhibits acute kidney injury-induced TCMK-1 cell apoptosis via activating the PPAR gamma signalling pathway
Molecular Omics ( IF 3.0 ) Pub Date : 2020-08-13 , DOI: 10.1039/d0mo00056f
Deyu Xu ₁ , Lei Shen , Ling Zhou , Wengang Sha , Jing Yang , Guoyuan Lu

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Acute kidney injury (AKI) is a frequently seen critical disorder in the clinic. The current research aimed to examine the role of hydroxyacid oxidase 2 (FABP7) in AKI-induced cell apoptosis. A total of 289 overlapping genes were used to perform gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses and to construct a protein–protein interaction (PPI) network using the DAVID database and Cytoscape software. The 10 hub genes of the PPI network were screened out using the cytohubba plug-in of Cytoscape software. FABP7 represented both the differentially expressed gene (DEG) from the GSE44925 and GSE62732 datasets and the top hub gene of the PPI network. The results of the PAS assay showed that FABP7 knockout in vivo aggravated lipopolysaccharide (LPS)-induced AKI. Meanwhile, LPS inhibited cell viability and the expression of FABP7, PPARγ, PPARα, PTEN and p27kip1, and increased the TNF-α level, and cleaved caspase-3/-9 expression and the phosphorylation of PTEN in vitro. FABP7 overexpression reversed the effects of LPS on inhibiting cell viability and proliferation, promoting cell apoptosis, increasing the expression of FABP7, PPARγ, PTEN and p27kip1, and reducing cleaved caspase-3/-9 expression and the phosphorylation of PTEN, but had no influence on PPARα expression. The PPARγ signal pathway inhibitors blocked the protective effect of FABP7 overexpression in LPS-treated TCMK-1 cells, while the PPARγ signal pathway activator inhibited the harmful effect of FABP7 inhibition in LPS-treated TCMK-1 cells. In conclusion, FABP7 overexpression inhibited the AKI-induced cell apoptosis and promoted the proliferation through activating the PPARγ signal pathway in vivo and in vitro.

中文翻译：

FABP7上调通过激活PPARγ信号通路抑制急性肾损伤诱导的TCMK-1细胞凋亡

急性肾损伤 (AKI) 是临床上常见的严重疾病。目前的研究旨在检查羟酸氧化酶 2 (FABP7) 在 AKI 诱导的细胞凋亡中的作用。总共使用 289 个重叠基因进行基因本体 (GO) 和京都基因和基因组百科全书 (KEGG) 通路富集分析，并使用 DAVID 数据库和 Cytoscape 软件构建蛋白质 - 蛋白质相互作用 (PPI) 网络。使用Cytoscape软件的cytohubba插件筛选出PPI网络的10个hub基因。FABP7 代表来自 GSE44925 和 GSE62732 数据集的差异表达基因 (DEG) 和 PPI 网络的顶部枢纽基因。PAS 检测结果表明 FABP7体内敲除加重脂多糖 (LPS) 诱导的 AKI。同时，LPS抑制细胞活力和FABP7、PPARγ、PPARα、PTEN和p27kip1的表达，增加TNF-α水平，裂解caspase-3/-9的表达和体外PTEN的磷酸化. FABP7过表达逆转LPS抑制细胞活力和增殖，促进细胞凋亡，增加FABP7、PPARγ、PTEN和p27kip1的表达，降低cleaved caspase-3/-9表达和PTEN磷酸化的作用，但无影响PPARα 表达。PPARγ信号通路抑制剂阻断了LPS处理的TCMK-1细胞中FABP7过表达的保护作用，而PPARγ信号通路激活剂则抑制了LPS处理的TCMK-1细胞中FABP7抑制的有害作用。总之，FABP7过度表达抑制了AKI诱导的细胞凋亡，并通过激活PPARγ信号通路促进增殖的体内和体外。

更新日期：2020-08-13

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