Maternal exposure to traffic pollutant causes impairment of spermatogenesis and alterations of genome-wide mRNA and microRNA expression in F2 male mice

Male spermatogenesis dysfunctions are associated with environmental pollutants, but the detailed mechanisms remain poorly understood. In this study, healthy C57BL/6 J mice were used to establish an animal model of maternal exposure to traffic pollutant during pregnancy, and the toxic effects on the reproductive system of F2 male mice were analysed using mRNA and miRNA microarray. Our results showed that 54 miRNAs and 1927 mRNAs were significantly altered in the exposed group. Gene Ontology (GO) analysis revealed that the most significant GO terms for biological process, molecular function and cellular component were myeloid cell differentiation, growth factor binding and main axon. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis demonstrated that the biosynthesis of amino acids was the most significant pathway and that the cytokine-cytokine receptor interaction was the most abundant pathway (37 genes). Protein-protein interaction (PPI) and the miRNA-mRNA network were constructed with Cytoscape. The hub genes, Tnf, Il10 and Gapdh, were closely related to immuno-regulation and their miRNA regulators were reversely changed. Together, our results indicate that maternal exposure to traffic pollutant can cause spermatogenesis damage in F2 male mice possibly through the destroyed immunoprivileged environment in testis mediated by the aberrant expression of miRNA and mRNA.