Abstract
Acute kidney injury (AKI) is a critical clinical disease characterized by an acute decrease in renal function. Long non-coding RNAs (LncRNAs) are important in AKI. This study aimed to explore the mechanism of lncRNA Kcnq1ot1 in AKI by sponging microRNA (miR)-204-5p as a competitive endogenous RNA (ceRNA). AKI mouse model and hypoxia/reoxygenation (H/R) model of human kidney (HK) cells were established. Kcnq1ot1 expression, cell proliferation, and apoptosis were measured. Binding relations among Kcnq1ot1, miR-204-5p, and NLRP3 were verified. Pathological changes and cell apoptosis were detected. The results showed that Kcnq1ot1 was highly expressed in the AKI model in vivo and in vitro. Kcnq1ot1 knockdown promoted cell proliferation and prevented apoptosis and inflammation. Furthermore, Kcnq1ot1 inhibited miR-204-5p expression by competitively binding to miR-204-5p in HK-2 cells. miR-204-5p targeted NLRP3 and NLRP3 overexpression averted the inhibiting effect of miR-204-5p on apoptosis and inflammation in HK-2 cells in vitro. Kcnq1ot1 knockdown in vivo promoted miR-204-5p expression, inhibited NLRP3 inflammasome activation, reduced levels of SCr, BUN, and KIM-1, and thus alleviated AKI and reduced apoptosis. In summary, silencing lncRNA Kcnq1ot1 inhibited AKI by promoting miR-204-5p and inhibiting NLRP3 inflammasome activation.
Highlights
Acute kidney injury (AKI), known as acute renal failure, is a group of clinical conditions characterized by sudden decreases in serum creatinine (SCr) and urine output which suggest a rapid drop in renal function-glomerular filtration rate (Levey and James, 2017; Ronco et al, 2019)
EnzymeLinked Immunosorbent Assay (ELISA) showed that compared with the blank group, levels of tumor necrosis factor-α (TNF-α), IL-6, and IL-1β were increased while IL-10 level was decreased in the H/R group (Figure 1D)
Reverse transcription-quantitative polymerase chain reaction showed that Kcnq1ot1 expression was increased in the H/R group compared with the blank group (Figure 1E)
Summary
Acute kidney injury (AKI), known as acute renal failure, is a group of clinical conditions characterized by sudden decreases in serum creatinine (SCr) and urine output which suggest a rapid drop in renal function-glomerular filtration rate (Levey and James, 2017; Ronco et al, 2019). The incidence of AKI has been increasing recently and the morbidity and mortality rates remain high (Negi et al, 2018). AKI could lead to long-term outcomes including. Silencing Kcnq1ot Alleviates AKI chronic kidney diseases or end-stage kidney diseases and cardiovascular conditions (Kashani et al, 2017). No interventions are available, and successful and sustainable care bundles are needed for AKI prevention and management (Vanmassenhove et al, 2017; Moore et al, 2018). The exploration of therapeutic targets for AKI is important and in urgent need
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