Abstract

Inflammation and renal cell apoptosis participate in sepsis-induced acute kidney injury. Previous research found the upregulation of long non-coding RNA Linc-KIAA1737–2 in hypoxia- or inflammation-challenged human proximal tubular epithelial cells, but its role in sepsis-induced acute kidney injury is underexplored. In this research, we found that Linc-KIAA1737–2 could be upregulated in HK-2 human proximal tubular epithelial cells by LPS treatment, and knock-down of this lncRNA significantly attenuated LPS-induced apoptosis in HK-2 cells, while its overexpression showed opposite effect. MiR-27a-3p was confirmed to interact with Linc-KIAA1737–2 in HK-2 cells by RNA pull-down and dual-luciferase assay. MiR-27a-3p mimic transfection significantly attenuated LPS-induced HK-2 cell apoptosis by downregulating the protein levels of TLR4 and NF-κB, which was overturned by overexpression of Linc-KIAA1737–2. Our results suggested that Linc-KIAA1737–2 could promote LPS-induced apoptosis in HK-2 cells, and presumably sepsis-induced acute kidney injury, by regulating the miR-27a-3p/TLR4/NF-κB axis.

Details

Title
Linc-KIAA1737–2 promoted LPS-induced HK-2 cell apoptosis by regulating miR-27a-3p/TLR4/NF-κB axis
Author
Hu, Ming 1 ; Wei, Jing 2 ; Liu, Yang 3 ; Xu, Jianhua 4 ; He Zhaofeng 5 ; Li, Haiyuan 4 ; Chao, Ning 4 ; Lu, Shijun 4 

 Zhejiang University, School of Medicine, Department of Anesthesiology, Sir Run Run Shaw Hospital, Hangzhou, China (GRID:grid.13402.34) (ISNI:0000 0004 1759 700X) 
 Qingdao Ninth People’s Hospital, Department of General practice, Qingdao, People’s Republic of China (GRID:grid.13402.34) 
 The Affiliated Central Hospital to Chongqing University, Department of Neurology, Chongqing Emergency Medical Center, Chongqing, China (GRID:grid.190737.b) (ISNI:0000 0001 0154 0904) 
 Shandong Province Linyi Central Hospital, Department of Critical Care Medicine, Linyi, China (GRID:grid.190737.b) 
 Shandong Province Juxian People’s Hospital, Department of Critical Care Medicine, Juxian, China (GRID:grid.190737.b) 
Pages
393-403
Publication year
2021
Publication date
Aug 2021
Publisher
Springer Nature B.V.
ISSN
0145-479X
e-ISSN
1573-6881
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2560480796
Copyright
© The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.