Abstract
Background and aimAcute kidney injury (AKI) is a common complication of sepsis. Long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) plays a vital role in various diseases, including AKI. This study aimed to investigate the function and mechanism of NEAT1 in sepsis-induced AKI.Materials and methodsA septic AKI model was established by treating HK-2 cells with lipopolysaccharide (LPS). The levels of NEAT1 and miR-22-3p were measured by quantitative real-time PCR. Cell apoptosis was assessed by flow cytometry. The levels of apoptosis-related protein and autophagy-related factors were examined by the western blot assay. An enzyme-linked immunosorbent assay was used to calculate the contents of inflammatory factors. The interaction between NEAT1 and miR-22-3p was validated by dual-luciferase reporter assay, RNA immunoprecipitation assay, and RNA pull-down assay. The levels of nuclear factor (NF)-κB pathway-related proteins were evaluated by the western blot assay.ResultsNEAT1 was upregulated, while miR-22-3p was downregulated in patients with sepsis and in LPS-stimulated HK-2 cells. LPS treatment triggered cell apoptosis, autophagy, and inflammatory response in HK-2 cells. NEAT1 knockdown attenuated LPS-induced cell injury. NEAT1 modulated LPS-triggered cell injury by targeting miR-22-3p. Furthermore, NEAT1 regulated the NF-κB pathway by modulating miR-22-3p.ConclusionDepletion of NEAT1 alleviated sepsis-induced AKI via regulating the miR-22-3p/NF-κB pathway.
Highlights
Sepsis is defined as a syndrome of the dysregulated host response to infection, resulting in life-threatening organ dysfunction [1]
The results revealed that nuclear-enriched abundant transcript 1 (NEAT1) expression was dramatically increased (Figure 1A), while the miR-22-3p expression was significantly decreased in patients with sepsis compared with healthy controls (Figure 1B)
We investigated the levels of NEAT1 and miR-22-3p in LPS-induced HK-2 cells
Summary
Sepsis is defined as a syndrome of the dysregulated host response to infection, resulting in life-threatening organ dysfunction [1]. Sepsis is one of the major causes of the global burden of diseases, leading to approximately 8 million deaths every year [2]. Acute kidney injury (AKI) has been recognized as a fatal complication of the illness; more than 50% of AKI are caused by sepsis [3]. AKI caused by sepsis is closely related to the high mortality of up to 60–80% [4]. Numerous studies have investigated the pathogenesis of sepsisinduced AKI, its pathophysiological mechanisms are still complex and have not been fully understood [5]. It is imperative to seek novel biomarkers for sepsisinduced AKI
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
