Dysregulation of HULC promotes contrast-induced nephropathy (CIN) via regulating signaling pathway of micorRNA-512 and prostaglandin E1 (PGE1)

Autor: Liang Zhang, Pan Li, Bi-li Zhang, Man-li Yu, Rong-liang Xu, Hong Wu, Shao-ping Chen
Rok vydání: 2020
Předmět:
DOI: 10.21203/rs.3.rs-19040/v1
Popis: Background It has been shown that contrast-induced nephropathy (CIN) could be attenuated by the administration of PGE1. As an enzyme responsible for the production of PGE1, PTGS1 is confirmed in this study as a miR-512 target. Meanwhile, HULC has been identified as a competing endogenous RNA of miR-512. Therefore, in this study, we tested the diagnostic value of HULC and miR-512 in subjects with or without CIN. In addition, we evaluated the regulatory relationship among HULC, miR-512, PTGS1 and PGE1 in vitro. Methods We enrolled 320 patients with coronary heart disease and divided them into a CIN group and a non-CIN group. Subsequently, we detected the differential expression of miR-512, HULC and PGE1 in the two groups. We also used a dual luciferase reporter assay to evaluate the regulatory relationship among HULC, miR-512, PTGS1 and PGE1 in THP-1 cells. Results In patients with CIN, the expression levels of HULC and PGE1 were lower, but the expression level of miR-512 was higher. MiR-512 could directly bind to and negatively regulate the expression of PTGS1 and HULC. The expression of HULC is positively correlated with the expression of PTGS1 and PGE1, while negatively correlated with the expression of miR-512. Conclusions MiR-512 is highly expressed in patients with CIN and promotes the progression of CIN by negatively regulating the expression of PTGS1 and HULC.
Databáze: OpenAIRE