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Lung microRNA Profiling Across the Estrous Cycle in Ozone-exposed Mice
Published on: January 7, 2019
Single-cell transcriptomics unveils PM2.5 exposure-induced mouse reproductive damage linked to embryonic
Yingdong Liu1, Haixin Liang1, Wenqiang Liu1
1Centre for Assisted Reproduction of Shanghai First Maternity and Infant Hospital, Shanghai Key Laboratory of Maternal Fetal Medicine, Clinical and Translational Research Center of Shanghai First Maternity and Infant Hospital, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Shanghai Key Laboratory of Signaling and Disease Research, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China.
Abstract:
This study employed C57BL/6 male mice to examine the effects of PM2.5 exposure on male reproductive function and early embryonic development. Single-cell transcriptomic analysis revealed significant DNA damage and metabolic dysregulation in the testicular tissues of PM2.5-exposed mice, starting at the undifferentiated spermatogonia stage. Untargeted metabolomics further identified metabolic disturbances in sperm, with notable alterations in key pathways, including galactose metabolism, glycine, serine, and threonine metabolism, and nucleotide metabolism. PM2.5 exposure significantly impaired sperm motility, thereby reducing its fertilizing capacity. Although the blastocyst formation rate in the PM2.5-exposed group did not differ significantly from that of the Control group, clear developmental delays were observed in peri-implantation embryos, accompanied by substantial transcriptomic abnormalities. Notably, pronounced dysregulation in differentially expressed genes was already evident at the 2-cell and blastocyst stages, suggesting that PM2.5 exposure may disrupt subsequent developmental processes by altering gene expression patterns in pre-implantation embryos.
