eISSN: 1644-4124
ISSN: 1426-3912
Central European Journal of Immunology
Current issue Archive Manuscripts accepted About the journal Special Issues Editorial board Abstracting and indexing Subscription Contact Instructions for authors Publication charge Ethical standards and procedures
Editorial System
Submit your Manuscript
SCImago Journal & Country Rank
Search
1/2022
vol. 47
 
Share:
Send email
Share:
abstract:
Experimental immunology

Downregulation of lncRNA NEAT1 alleviates sepsis-induced acute kidney injury

Yuhua Zhou
1
,
Yihui Wang
1
,
Qingtian Li
2
,
Ke Dong
2
,
Chunyan Chen
2
,
Enqiang Mao
1
,
Weisong Jiang
1

  1. Department of Emergency, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China
  2. Key Laboratory of Parasite and Vector Biology, Ministry of Health, Chinese Center for Tropical Disease Research, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China
Cent Eur J Immunol 2022; 47 (1): 8-19
DOI: https://doi.org/10.5114/ceji.2022.115628
Online publish date: 2022/04/20
View full text Get citation
 
PlumX metrics:
Sepsis-induced acute kidney injury (AKI) is one of the important causes of increased mortality in sepsis patients. Long non-coding RNA (lncRNA) is believed to play a vital function in the progression of AKI. However, the mechanism of nuclear enriched abundant transcript 1 (NEAT1) has not been fully elucidated. NEAT1 was overexpressed and miR-22-3p was underexpressed in sepsis patients and lipopolysaccharide (LPS)-induced AKI cell models. Knockdown of NEAT1 could promote viability and suppress apoptosis and the inflammatory response in LPS-induced HK2 cells. MiR-22-3p could be sponged by NEAT1, and its inhibitor reversed the inhibition effect of NEAT1 silencing on LPS-induced HK2 cell injury. CXCL12 could be targeted by miR-22-3p, and its overexpression reversed the suppression effect of miR-22-3p on LPS-induced HK2 cell injury. Silenced NEAT1 could restrain the activity of the NF-B signaling pathway, and miR-22-3p inhibitor or CXCL12 overexpression could reverse this effect. In addition, NEAT1 knockdown alleviated the inflammation response of cecal ligation and puncture (CLP) mouse models. In summary, our data showed that NEAT1 promoted LPS-induced HK2 cell injury via regulating the miR-22-3p/CXCL12/NF-B signaling pathway, suggesting that NEAT1 knockdown might be a potential pathway for alleviating sepsis-induced AKI.
keywords:

sepsis, acute kidney injury, NEAT1, miR-22-3p, CXCL12
Termedia
About us Contact
Copyright notice Privacy policy Advertising policy Contact us
Quick links
Journals Books eBooks Events
© 2024 Termedia Sp. z o.o.
Developed by Bentus.