LncRNA TapSAKI promotes inflammation injury in HK-2 cells and urine derived sepsis-induced kidney injury.
J Pharm Pharmacol
; 71(5): 839-848, 2019 May.
Article
em En
| MEDLINE
| ID: mdl-30666657
ABSTRACT
OBJECTIVE:
To explore the possible mechanism of lncRNA TapSAKI in urine derived sepsis-induced kidney injury. MATERIALS ANDMETHODS:
In vivo urine-derived sepsis (US) rat model and in vitro LPS-induced HK-2 cells were established, and TapSAKI, miR-22, PTEN, TLR4 and p-p65 expressions were detected by qRT-PCR and western blot. RNA precipitation and RNA pull-down were performed to confirm the interaction between TapSAKI and miR-22.RESULTS:
TapSAKI was up-regulated, miR-22 was down-regulated, PTEN, TLR4 and p-p65 expressions, and inflammatory factors TNF-α and IL-6 levels were up-regulated in kidney tissue of US rats and LPS-induced HK-2 cells. In addition, TapSAKI interacted with miR-22, and negatively modulate miR-22 expression. We also observed TapSAKI promoted PTEN expression, TLR4/NF-κB pathway related proteins TLR4 and p-p65, and apoptosis protein cleaved-caspase-3 through negatively regulating miR-22. Further experiments proved TapSAKI/miR-22/TLR4/NF-κB pathway could promote HK-2 cell apoptosis. Finally, in vivo experiments showed TapSAKI knockdown negatively regulated miR-22 and positively regulate PTEN, decreased renal function indicators blood urea nitrogen and serum creatinine, and reduced TNF-α and IL-6.CONCLUSION:
TapSAKI was elevated in urine derived sepsis-induced kidney injury, and promoted HK-2 cell apoptosis and inflammatory response through miR-22/PTEN/TLR4/NF-κB pathway.Palavras-chave
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Sepse
/
RNA Longo não Codificante
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article