LncRNA NEAT1 regulated inflammation and apoptosis in a rat model of sepsis-induced acute kidney injury via MiR-27a-3p/TAB3 axis

This study explored the mechanism of NEAT1 in sepsis-induced AKI rats. Cecal ligation punctures (CLP)-induced AKI rats were injected with siRNA-NEAT1 lentivirus. Kidney histopathology and apoptosis were evaluated via hematoxylin-eosin and TUNEL staining, respectively. ELISA determined the levels of...

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Published in:Bioscience, biotechnology, and biochemistry biotechnology, and biochemistry, 2020-11, Vol.84 (11), p.2215-2227
Main Authors: Wang, Jiasheng, Chen, Yong, Tang, Ze, Hu, Dabi, Yao, Caoyuan, Yang, Lei
Format: Article
Language:English
Subjects:
acute kidney injury
Acute Kidney Injury - etiology
Acute Kidney Injury - genetics
Acute Kidney Injury - metabolism
Animals
Apoptosis - genetics
Carrier Proteins - metabolism
Disease Models, Animal
HEK293 Cells
Humans
Inflammation - genetics
Inflammation - metabolism
inflammatory response
MicroRNAs - genetics
miR-27a-3p
NEAT1
Nerve Tissue Proteins - metabolism
RNA, Long Noncoding - genetics
Sepsis - complications
TAB3
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Summary:This study explored the mechanism of NEAT1 in sepsis-induced AKI rats. Cecal ligation punctures (CLP)-induced AKI rats were injected with siRNA-NEAT1 lentivirus. Kidney histopathology and apoptosis were evaluated via hematoxylin-eosin and TUNEL staining, respectively. ELISA determined the levels of Blood urea nitrogen (BUN), serum creatinine (SCr), neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), TNF-α, Interleukin (IL)-1β, and IL-6. Colorimetry measured malondialdehyde (MDA), superoxide dismutase (SOD) activities. qPCR analyzed NEAT1, miR-27a-3p, TAB3, Bcl-2, and Bax expressions. siNEAT1 reversed the promotive effect of CLP on kidney histopathological injury, and BUN, SCr, NGAL, KIM-1, TNF-α, IL-1β, IL-6, MDA, and Bax levels and apoptosis, but raised CLP-downregulated SOD and Bcl-2 levels. NEAT1 sponged miR-27a-3p which targeted TAB3. siNEAT1 upregulated miR-27a-3p and downregulated TAB3 expression. TAB3 overexpression reversed the inhibitory effect of siNEAT1 on the LPS-induced apoptosis of HK-2 cells. siNEAT1 alleviated sepsis-induced AKI in rats and LPS-induced sepsis of cells via miR-27a-3p/TAB3 axis. siNEAT1 inhibited inflammation and apoptosis in a rat model of sepsis-induced acute kidney injury via regulating miR-27a-3p/TAB3 axis
ISSN:0916-8451
1347-6947
DOI:10.1080/09168451.2020.1792760