LncRNAL20992 Regulates Apoptotic Proteins to Promote Lead-induced Neuronal Apoptosis.

3 years ago

LncRNAL20992 Regulates Apoptotic Proteins to Promote Lead-induced Neuronal Apoptosis.

Cheng, Nan, Li, Jiang, Chen, Ling, Jia, Liu, Dai, Xu, Yang, Zhang

Lead is a heavy metal pollutant that is widely present in the environment and can seriously harm human health, especially the nervous system. Long noncoding RNAs (lncRNAs) play important roles in many physiological and pathological processes; however, there remains a lack of in-depth studies on the molecular mechanisms associated with lead neurotoxicity. Here, our results showed that lead exposure inhibited cell proliferation and promoted cell apoptosis. We observed that lncRNAL20992 was significantly upregulated in a lead-induced neuronal-injury cell model according to quantitative reverse transcription polymerase chain reaction. Silencing lncRNAL20992 revealed its significant functions involved in promoting cell apoptosis and inhibiting cell proliferation according to cell-counting kit-8, EdU assay, terminal deoxynucleotidyl transferase dUTP nick-end labeling and western-blot. To elucidate the molecular mechanisms of lncRNAL20992, we used RNA-pulldown mass spectrometry combined with bioinformatics analysis to discover four proteins (AIFM1, HSP7C, GRP78, and LMNA) that interacted with lncRNAL20992. Western blot analysis indicating lncRNAL20992 involvement in lead-induced neuronal injury mediated by the four proteins. Our study constitutes the first investigation of the functions and related mechanisms of lncRNAL20992 and offered valuable insight into understanding the roles of lncRNA in lead-induced neurotoxicity.

Publisher URL: http://doi.org/10.1093/toxsci/kfx203

DOI: 10.1093/toxsci/kfx203