Aims: Paraquat Poisoning (PQ) can cause illness and death, and its main causes of mortality are acute respiratory failure and lung fibrosis. Early recognition of this condition and early treatment are vital. Thus, it is of importance to target the key genes controlling pathogenesis in the early stage of PQ.
Main methods: C57BL/6 mice were used for Paraquat intragastric administration as a model of PQ. Following a gene chip-based screening, the change of gene expression in the lung was further validated by bioinformatic analyses, co-expression network construction and real-time RT-PCR, Western blot and immunofluorescence assays.
Key findings: 2287 genes with differential expression were identified at the very early stage of PQ. From these, 76 genes that were linked to mitochondrion function were further pursued. Among these genes, PSTK was a phosphorylase kinase which serves a protective role in oxidative stress lung damage. PSTK was the central gene in a 30-gene network that is important for mitochondrial complex I assembly, mitochondrial apoptosis and mitochondrial fatty acid beta-oxidation, suggesting that they could conceivably be related to the pathogenesis of PQ induced lung damage. Lastly, we confirmed that PSTK was lowered in rodent lungs following PQ.
Significance: PSTK emerges as a central gene in a network of mitochondrial function genes in PQ exposed mice. The functional role of PSTK in PQ induced lung injury warrants further examination.
Keywords: Microarray; PSTK; Paraquat Poisoning.
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