Long non-coding RNA CASC2 ameliorates sepsis-induced acute kidney injury by regulating the miR-155 and NF-κB pathway

Sepsis is a systemic inflammatory response syndrome that can cause multiple-organ damage, including acute kidney injury (AKI). Studies have shown that the long non-coding RNA cancer susceptibility candidate 2 (CASC2) is involved in the occurrence and development of multiple human diseases, although...

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Vydáno v:	International journal of molecular medicine Ročník 45; číslo 5; s. 1554 - 1562
Hlavní autoři:	Wang, Min, Wei, Jilou, Shang, Futai, Zang, Kui, Ji, Ting
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	Greece D.A. Spandidos 01.05.2020 Spandidos Publications UK Ltd
Témata:	acute kidney injury Acute Kidney Injury - genetics Adult Aged Animals Apoptosis Apoptosis - genetics Cancer cancer susceptibility candidate 2 Cell growth Cell Line Cell Survival - genetics Down-Regulation - genetics Female Gene Expression Regulation, Neoplastic - genetics HEK293 Cells Humans Inflammation - genetics Kidneys Laboratory animals long non-coding RNA Male Males Mice Mice, Inbred BALB C microRNA-155 MicroRNAs MicroRNAs - genetics Middle Aged NF-kappa B - genetics nuclear factor-κB Oxidative Stress - genetics Sepsis Sepsis - genetics Tumor necrosis factor-TNF Tumor Suppressor Proteins - genetics Up-Regulation - genetics Young Adult
ISSN:	1107-3756, 1791-244X, 1791-244X
On-line přístup:	Získat plný text
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Popis
Shrnutí:	Sepsis is a systemic inflammatory response syndrome that can cause multiple-organ damage, including acute kidney injury (AKI). Studies have shown that the long non-coding RNA cancer susceptibility candidate 2 (CASC2) is involved in the occurrence and development of multiple human diseases, although its expression and role in AKI has not yet been reported. The present study demonstrated that the expression of CASC2 was significantly decreased in the serum of patients with sepsis compared with healthy subjects. In addition, the CASC2 level was negatively associated with the severity of AKI. Further experiments revealed that CASC2 promoted cell viability and inhibited inflammatory factor secretion, apoptosis and oxidative stress in lipopolysaccharide-stimulated human renal tubular epithelial HK-2 cells. Importantly, the current study observed that CASC2 was negatively associated with a pro-inflammatory microRNA (miR)-155. In addition, the upregulation of CASC2 significantly suppressed the nuclear factor κB (NF-κB) signaling pathway. In conclusion, the results of the present study suggested that CASC2 may serve as a potential target for treating sepsis-induced AKI by inhibiting the miR-155 and NF-κB pathway-mediated inflammation.
Bibliografie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23
ISSN:	1107-3756 1791-244X 1791-244X
DOI:	10.3892/ijmm.2020.4518