PTEN expression was down-regulated in population occupational mercury exposure and promote cell apoptosis via PI3K/AKT pathway

Abstract Background: Mercury has different levels of toxicity to various organ systems of the human body. Therefore, it is very important to research the molecular differences and functional mechanisms of mercury exposure for the early prevention and treatment of occupational mercury poisoning. Method:The subjects of the population study were on-the-job workers in a thermometer manufacturing plant in Jiangsu Province in 2016. According to the basic information collected, 40 people in the high concentration mercury exposure group and 40 people in the low concentration mercury exposure group (control group) were matched, and the blood of each person was collected. Through bioinformatics analysis of gene expression microarray results, the genes related to mercury exposure were initially screened out. The qRT-PCR was used to verify the initial screening of differential expression genes (DEGs) to identify the differential genes of mercury exposure. Mercury exposure differential genes were verified in 293T model cells, and the molecular functions and mechanisms of mercury exposure differential genes were analyzed by qRT-PCR, Western blot, siRNA transfection and ELISA. Results: Compared with the control group, the expression level of PTEN in the high-concentration mercury exposure group was 21.86% of that in the control group. The result of correlation analysis showed that the relative expression levels of PTEN and RNF2 genes were negatively correlated with the urine mercury value. The expression of PTEN was down-regulated, and the expression of PI3K, AKT and IL-6protein was increased in the mercury-infected 293T cell model. Conclusions:The results showed that mercury exposure could down-regulate the PTEN gene, activate the PI3K/AKT regulatory pathway, increase the expression of inflammatory factors, and thus cause renal inflammation.