The novel regulatory role of miR-101a in CRH expression following low-concentration DEHP exposure in zebrafish embryos
摘要
Di (2-ethylhexyl) phthalate (DEHP) is extremely application in industrial production. DEHP and its metabolites can induce epigenetic changes, such as selective gene expression regulation and post-transcriptional gene regulation, leading to adverse outcome pathways in living organisms. Our findings, bioinformatics tools, and miRNA-mRNA prediction suggested that corticotropin-releasing hormone (CRH) could be miR-101a’s target gene. Although the regulatory relationship between miR-101a and CRH has not been experimentally established, the present study aimed to investigate this interaction in zebrafish embryos exposed to low concentrations of DEHP. Both DLR™ and DFP™ reporter assays confirmed the biological association between miR-101a and CRH mRNA. Validation experiments revealed that overexpression or knockdown of miR-101a in ZF4 cells resulted in changes in CRH mRNA expression. These findings represent that miR-101a adversely impacts CRH at the levels of mRNA.This study improves the discovery of the molecular toxicology of DEHP exposure, and miR-101a is predicted to be a novel toxicological biomarker for chemical hazards.