Journal article
Downregulation of lncRNA NEAT1 alleviates sepsis-induced acute kidney injury
Central-European journal of immunology, Vol.47(1), pp.8-19
2022
DOI: 10.5114/ceji.2022.115628
PMCID: PMC9115601
PMID: 35600150
Abstract
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-κB 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-κB signaling pathway, suggesting that NEAT1 knockdown might be a potential pathway for alleviating sepsis-induced AKI.
Details
- Title: Subtitle
- Downregulation of lncRNA NEAT1 alleviates sepsis-induced acute kidney injury
- Creators
- Yuhua Zhou - Ruijin HospitalYihui Wang - Ruijin HospitalQingtian Li - Shanghai Jiao Tong UniversityKe Dong - National Institute for Parasitic DiseasesChunyan Chen - Shanghai Jiao Tong UniversityEnqiang Mao - Ruijin HospitalWeisong Jiang - Ruijin Hospital
- Resource Type
- Journal article
- Publication Details
- Central-European journal of immunology, Vol.47(1), pp.8-19
- DOI
- 10.5114/ceji.2022.115628
- PMID
- 35600150
- PMCID
- PMC9115601
- NLM abbreviation
- Cent Eur J Immunol
- ISSN
- 1426-3912
- eISSN
- 1644-4124
- Publisher
- Termedia Publishing House; POZNAN
- Grant note
- Natural Science Foundation of Shanghai: 17ZR1415900 Medical Guidance Project of Shanghai Science and Technology Commission: 18411966400
This work was supported by the Natural Science Foundation of Shanghai [No. 17ZR1415900] and the Medical Guidance Project of Shanghai Science and Technology Commission [No. 18411966400].
- Language
- English
- Date published
- 2022
- Academic Unit
- Internal Medicine
- Record Identifier
- 9984696651502771
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