Linc-KIAA1737–2 promoted LPS-induced HK-2 cell apoptosis by regulating miR-27a-3p/TLR4/NF-κB axis
| Autor: | Chao Ning, Liu Yang, Ming Hu, Haiyuan Li, Jian‐Hua Xu, Jing Wei, Zhaofeng He, Shi‐Jun Lu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Lipopolysaccharides Physiology Inflammation Apoptosis Transfection Article NF-κB 03 medical and health sciences chemistry.chemical_compound Linc-KIAA1737–2 0302 clinical medicine Downregulation and upregulation Sepsis medicine Humans TLR4 miR-27a Chemistry Acute kidney injury NF-kappa B RNA Cell Biology medicine.disease Cell biology MicroRNAs 030104 developmental biology 030220 oncology & carcinogenesis RNA Long Noncoding medicine.symptom |
| Zdroj: | Journal of Bioenergetics and Biomembranes |
| ISSN: | 1573-6881 0145-479X |
| Popis: | 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. Supplementary Information The online version contains supplementary material available at 10.1007/s10863-021-09897-1. |
| Databáze: | OpenAIRE |
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