Abstract
Acute kidney injury (AKI) is one of the most common complications affecting hospitalized patients associated with an extremely high mortality rate. However, the underlying pathogenesis of AKI remains unclear that largely limits its effective management in clinic. Increasing evidence demonstrated the importance of long non-coding RNAs (lncRNAs) in the pathogenesis of AKI, because of their regulatory roles in transcription, translation, chromatin modification, and cellular organization. Here, we reported a new role of LRNA9884 in AKI. Using experimental cisplatin-induced AKI model, we found that LRNA9884 was markedly up-regulated in the nucleus of renal tubular epithelium in mice with AKI. We found that silencing of LRNA9884 effectively inhibited the production of inflammatory cytokines MCP-1, IL-6, and TNF-α in the mouse renal tubular epithelial cells (mTECs) under IL-1β stimulation in vitro. Mechanistically, LRNA9884 was involved into NF-κB-mediated inflammatory cytokines production especially on macrophage migration inhibitory factor (MIF). Collectedly, our study suggested LRNA9884 promoted MIF-triggered the production of inflammatory cytokines via NF-κB pathway after AKI injury. This study uncovered LRNA9884 has an adverse impact in AKI, and targeting LRNA9884 might represent a potential therapeutic target for AKI.
Highlights
Acute kidney injury (AKI) is defined as a sudden deterioration in kidney function over a short period of time
Inflammatory cytokines were up-regulated in the AKI kidneys such as IL1β and TNFα, indicated that activating inflammatory signals involved in cisplatin-induced AKI (Figure 1B)
AKI can gradually progress into chronic renal failure due to persistent inflammation and progressive fibrosis, in which significant amounts of inflammatory and pro-inflammatory cytokines are released causing disease progression (Kinsey et al, 2008; Chawla et al, 2011)
Summary
Acute kidney injury (AKI) is defined as a sudden deterioration in kidney function over a short period of time. Studies have reported that 3.2–21% of hospitalized patients and up to 50% of patients admitted to intensive care units develop AKI, with a mortality rate ranging from 40 to 60%. If there are other comorbidities with AKI, the incidence and mortality rates can be as high. Studies found that AKI significantly prolonged the length of a patient’s stay in hospital and significantly increased overall inpatient expenses (about $24 billion annually in the United States) (Silver et al, 2017). The cost required to treat AKI is comparable to treating other serious conditions such as stroke, pancreatitis and pneumonia. Taken together, these findings highlight the need for new therapies to treat this serious condition
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