Add like
Add dislike
Add to saved papers

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.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app