Pseudogene HMGN2P46 as a microRNA sponge to regulate HMGN2 expression via competing for miR-590-3p in severe acute pancreatitis

HMGN2 have functions in inflammatory response. However, the role of HMGN2 in severe acute pancreatitis (SAP) remains unclear. Here, our study was to discuss the role and regulatory mechanism ofHMGN2 in SAP. In this study, the SAP cell model of AR42J was used to study the function and mechanism of HMGN2 in SAP. The protein expression in cells and serums were examined by western blot and ELISA assay. qPCR was used to test the transcriptional RNA level. Cell viability were examined by Am assay. Luciferase assay was used to evaluate the interaction between gene and gene. Our results showed that HMGN2 was significantly upregulated in SAP patients. The database predicted and luciferase assay data indicated the HMGN2 was directly binding with miR-590-3p. ELISA, MTT and western blot experiments showed that the HMGN2 were promoted the cell proliferation, reduced the inflammation, and repressed the cell autophagy. Mechanism studies showed that the pseudogene HMGN2P46 level was positively correlated with HMGN2 and upregulated HMGN2 expression by competing for miR-590-3p in SAP. Taken together, all over these results showed upregulation of HMGN2 alleviates SAP, this process was regulated by HMGN2P46 competitively binding with miR-590-3p, which may provide a new insight for the treatment and intervention in SAP. Pseudogene HMGN2P46 was a miRNA sponge to regulate HMGN2 level by competing for miR-590-3p to alleviate the process of SAP. It provided a novel strategy for the diagnosis and treatment of severe acute pancreatitis.