Xinghan Tian1,2, Yongqiang Ji3, Yafeng Liang2, Jing Zhang1, Lina Guan4, Chunting Wang1. 1. Department of Critical Care Medicine, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, China. 2. Department of Critical Care Medicine, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong, China. 3. Department of Nephrology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong, China. 4. Department of Neurology Intensive Care Unit, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong, China.
Abstract
BACKGROUND: Acute kidney injury (AKI) shows several kinds of disorders, which acutely harm the kidney. However, the current medical methods have limited therapeutic effects. The present study aimed to find out the molecular mechanism of AKI pathogenesis, which may provide new insights for future therapy. METHODS: Bioinformatic analysis was conducted using the R language (AT&T BellLaboratories, University of Auckland, New Zealand) to acquire the differentially expressed long noncoding RNAs (lncRNAs) and messenger RNAs (mRNAs) in AKI. The expression levels of RNAs and related proteins in tissues and cells were detected by quantitative real-time PCR (qRT-PCR) and western blot. Dual-luciferase reporter gene assays were performed to verify the target relationship between microRNA (miRNA) and lncRNA as well as miRNA and mRNA. Flow cytometry and tunnel assay were used to detect the cell apoptotic rate in AKI. RESULTS: LINC00520, miR-27b-3p, and OSMR form an axis to regulate AKI. Knockdown of LINC00520 reduced acute renal injury both in vitro and in vivo. LINC00520 activated the PI3K/AKT pathway to aggravate renal ischemia/reperfusion injury, while upregulation of miR-27b-3p or downregulation of OSMR could accelerate the recovery of AKI. CONCLUSION: Overexpression of LINC00520 contributes to the aggravation of AKI by targeting miR-27b-3p/ OSMR.
BACKGROUND:Acute kidney injury (AKI) shows several kinds of disorders, which acutely harm the kidney. However, the current medical methods have limited therapeutic effects. The present study aimed to find out the molecular mechanism of AKI pathogenesis, which may provide new insights for future therapy. METHODS: Bioinformatic analysis was conducted using the R language (AT&T BellLaboratories, University of Auckland, New Zealand) to acquire the differentially expressed long noncoding RNAs (lncRNAs) and messenger RNAs (mRNAs) in AKI. The expression levels of RNAs and related proteins in tissues and cells were detected by quantitative real-time PCR (qRT-PCR) and western blot. Dual-luciferase reporter gene assays were performed to verify the target relationship between microRNA (miRNA) and lncRNA as well as miRNA and mRNA. Flow cytometry and tunnel assay were used to detect the cell apoptotic rate in AKI. RESULTS:LINC00520, miR-27b-3p, and OSMR form an axis to regulate AKI. Knockdown of LINC00520 reduced acute renal injury both in vitro and in vivo. LINC00520 activated the PI3K/AKT pathway to aggravate renal ischemia/reperfusion injury, while upregulation of miR-27b-3p or downregulation of OSMR could accelerate the recovery of AKI. CONCLUSION: Overexpression of LINC00520 contributes to the aggravation of AKI by targeting miR-27b-3p/ OSMR.