Cooperative application of transcriptomics and ceRNA hypothesis: LncRNA-107052630/miR-205a/G0S2 crosstalk is involved in ammonia-induced intestinal apoptotic injury in chicken

• Published in: Journal of hazardous materials Vol. 396; p. 122605
• Main Authors: Wang, Shengchen, Wang, Wei, Li, Xiaojing, Zhao, Xia, Wang, Yue, Zhang, Hongfu, Xu, Shiwen
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 05.09.2020
• Subjects: Ammonia; Ammonia - toxicity; Animals; Apoptosis; ceRNA; Chickens; Gene Regulatory Networks; jejunum; MicroRNAs - genetics; RNA, Long Noncoding - genetics; RNA, Messenger; Transcriptome; Ammonia; ceRNA; jejunum; Transcriptome; Apoptosis
• ISSN: 0304-3894; 1873-3336
• DOI: 10.1016/j.jhazmat.2020.122605

[Display omitted] •Transcriptomics and ceRNA network construction were applied to study NH3 toxicity.•46 lncRNAs and 30 microRNAs were differentially expressed after NH3 exposure.•NH3 caused apopotic injury of jejunum in chicken.•LncRNA-107052630/miR-205a/G0S2 crosstalk plays a crucial role in NH3 induced apoptosis. Ammonia (NH3), as a harmful gas from agricultural production, plays an important role in air pollution, such as haze. Although numerous researchers have paid attention to health damage through NH3 inhalation, the exhaustive mechanism of NH3 induced intestinal toxicity remains unclear. A genes crosstalk named competing endogenous RNAs (ceRNA) can explain many regulatory manners from the molecular perspective. However, few studies have attempted to interpret the injury mechanism of air pollutants to the organism via ceRNA theory. Here, we thoroughly investigated the lncRNA-associated-ceRNA mechanism in jejunum samples from a 42-days-old NH3-exposed chicken model through deep RNA sequencing. We observed the occurrence of apoptosis in jejunum, obtained 46 significantly dysregulated lncRNAs and 30 dysregulated miRNAs, and then constructed lncRNA-associated-ceRNA networks in jejunum. Importantly, a network regulating G0S2 in NH3-induced apoptosis was discovered. Research results showed that G0S2 was upregulated in jejunum of NH3-exposed group and was associated with activation of the mitochondrial apoptosis pathway. G0S2 antagonized the anti-apoptotic effect of Bcl2, which could be reversed by miR-205a. Meanwhile, lncRNA-107052630 acted as ceRNA to affect G0S2 function. These data provide new insight for revealing the biological effect of NH3 toxicity, as well as the environmental research.