Acute Kidney Injury

TUG1[LncRNA]

miR-494-3p[miRNA]

E-cadherin[mRNA]

HK-2 cell

Homo sapiens (human)

J Inflamm (Lond). 2021 Mar 4;18(1):12. doi: 10.1186/s12950-021-00278-4.

LncRNA TUG1 regulates the development of ischemia-reperfusion mediated acute kidney injury through miR-494-3p/E-cadherin axis.

ELISA;RT-PCR;Western blot;Flow Cytometry assay;luciferase assay;

BACKGROUND: Acute kidney injury (AKI) results from renal dysfunction caused by various causes, resulting in high mortality. The underlying mechanisms of ischemia-reperfusion (I/R) induced AKI is very complicated and needed for further research. Here, we sought to found out the functions of lncRNA TUG1 in I/R-induced AKI. METHODS: In vivo model was constructed by I/R-induced mice and in vitro model was constructed by hypoxia/reoxygenation (H/R)-induced HK-2 cell. Kidney tissue damage was evaluated through H&E staining in mice. Cell flow cytometry was used to detect the degree of apoptosis. TUG1, miR-494-3p and E-cadherin were determined both by RT-PCR and western blot. Dual luciferase assay was employed to validate the relationships between TUG1, miR-494-3p and E-cadherin. Inflammatory factors including IL-1β, TNFɑ and IL-6 were evaluated by ELISA. RESULTS: lncRNA TUG1 was decreased while miR-494-3p was elevated in vivo and in vitro. Overexpression of TUG1 or transfection with miR-494-3p inhibitor significantly alleviated cell apoptosis. MiR-494-3p directly targeted E-cadherin and TUG1 suppressed cell apoptosis via serving as a miR-494-3p sponge to disinhibit E-cadherin. CONCLUSION: lncRNA TUG1 alleviated I/R-induced AKI through targeting miR-494-3p/E-cadherin.