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DOI 10.1002/jcp.28422

Медицинская библиотека · Journal of cellular physiology · 2019

MicroRNA signature of air pollution exposure-induced congenital defects.

Li Zheng, Ma Jianqing, Bi Jiaqi, Guo Haiwei, Chan Matthew T V, Wu William K K, Wu Zhanyong, Shen Jianxiong

СтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

Air pollution exposure has been increasing extensively and there are evidence suggesting that exposure to air pollution during pregnancy can lead to congenital defects in the offspring. Recent findings suggested that microRNAs (miRNAs) might play important roles in the pathogenesis of developmental defects. However, the miRNAs profile pattern in the air pollution-exposed embryos remains unknown. RNA sequencing was performed to determine the differentially expressed miRNAs in the rat embryos (gestation day 9) with or without air pollution exposure. The potential functions and the associated mechanisms of these differentially expressed miRNAs were determined using Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and Gene Ontology (GO) analyses. The regulatory networks of mRNA-miRNA interactions were also reconstructed. As compared with the control group, a total of 291 miRNAs were differentially expressed in the rat embryos from the air pollution-exposed group, in which 204 and 87 miRNAs were significantly downregulated and upregulated, respectively. These miRNAs were predicted to deregulate mitotic spindle organization, cellular respiration, glycolate metabolism, and proteasome. Extensive regulation of target genes by miR-346, miR-504, miR-214-3p and miR-1224 was also predicted. Our results suggested that miRNAs may play crucial roles in the pathogenesis of air pollution-induced congenital spinal defects through deregulating multiple biological processes.

Для цитирования: Li Zheng, Ma Jianqing, Bi Jiaqi, Guo Haiwei, Chan Matthew T V, Wu William K K, Wu Zhanyong, Shen Jianxiong. MicroRNA signature of air pollution exposure-induced congenital defects.. Journal of cellular physiology. 2019. DOI: 10.1002/jcp.28422.

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