Abstract
Acute kidney injury (AKI) is a severe kidney disease defined by partial or abrupt loss of renal function. Emerging evidence indicates that non-coding RNAs (ncRNAs), particularly long non-coding RNAs (lncRNAs), function as essential regulators in AKI development. Here we aimed to explore the underlying molecular mechanism of the lncRNA H19/miR-130a axis for the regulation of inflammation, proliferation, and apoptosis in kidney epithelial cells. Human renal proximal tubular cells (HK-2) were induced by hypoxia/reoxygenation to replicate the AKI model in vitro. After treatment, the effects of LncRNA H19 and miR-130a on proliferation and apoptosis of HK-2 cells were investigated by CCK-8 and flow cytometry. Meanwhile, the expressions of LncRNA H19, miR-130a, and inflammatory cytokines were detected by qRT-PCR, western blot, and ELISA assays. The results showed that downregulation of LncRNA H19 could promote cell proliferation, inhibit cell apoptosis, and suppress multiple inflammatory cytokine expressions in HK-2 cells by modulating the miR-130a/BCL2L11 pathway. Taken together, our findings indicated that LncRNA H19 and miR-130a might represent novel therapeutic targets and early diagnostic biomarkers for the treatment of AKI.
Highlights
Acute kidney injury (AKI), characterized by persistent oliguria and elevated serum creatinine, is a frequent complication accompanied by high mortality, long-term hospitalization, and decreased kidney filtration function ability (Zafrani et al, 2016)
The results showed that downregulation of Long non-coding RNAs (LncRNAs) H19 could promote cell proliferation, inhibit cell apoptosis, and suppress multiple inflammatory cytokine expressions in HK-2 cells by modulating the miR-130a/BCL2L11 pathway
Our findings indicated that LncRNA H19 and miR-130a might represent novel therapeutic targets and early diagnostic biomarkers for the treatment of AKI
Summary
Acute kidney injury (AKI), characterized by persistent oliguria and elevated serum creatinine, is a frequent complication accompanied by high mortality, long-term hospitalization, and decreased kidney filtration function ability (Zafrani et al, 2016). Sepsis is a common cause of AKI, and previous studies found that severe sepsis could result in 60% AKI incidence clinically (Gómez and Kellum, 2016). The pathogenesis of sepsis-induced AKI includes inflammation, oxidative stress, and tubular epithelial response (Zhao et al, 2016). A common cause of AKI, may contribute to tubular epithelial cell necrosis and immune responses (Potteti et al, 2016). Elucidating the underlying mechanisms of AKI and exploring novel therapeutic targets or early diagnostic biomarkers are important for the treatment of AKI.
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