Long noncoding RNA distal-less homeobox 2 antisense 1 restrains inflammatory response and apoptosis of periodontal ligament cells by binding with microRNA-330-3p to regulate Ro60, Y RNA binding protein.
Arch Oral Biol
; 133: 105298, 2022 Jan.
Article
em En
| MEDLINE
| ID: mdl-34752991
OBJECTIVE: This study aims to investigate the role of long noncoding RNA distal-less homeobox 2 antisense 1 (DLX2-AS1) in lipopolysaccharide-induced inflammatory response and apoptosis of periodontal ligament cells (PDLCs). DESIGN: Lipopolysaccharide was used to induce inflammation response of PDLCs. The expression of DLX2-AS1, microRNA-330-3p and Ro60, Y RNA binding protein (RO60) in lipopolysaccharide-treated PDLCs was detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Enzyme linked immunosorbent assay (ELISA) was performed to evaluate the concentration of inflammatory cytokines in PDLCs after DLX2-AS1 overexpression or RO60 downregulation. The apoptosis of PDLCs after lipopolysaccharide treatment or indicated transfection was analyzed by flow cytometry analysis. The level of apoptosis-related proteins, Bax and Bcl-2, were examined by western blotting. The binding capacity between microRNA-330-3p and DLX2-AS1 (or RO60) was verified by luciferase reporter assays. RESULTS: DLX2-AS1 was downregulated in PDLCs after lipopolysaccharide treatment. DLX2-AS1 overexpression decreased the production of inflammatory cytokines and inhibited cell apoptosis. microRNA-330-3p bound with DLX2-AS1 and displayed high expression in lipopolysaccharide-induced PDLCs. In addition, the downregulation of RO60, a target gene of microRNA-330-3p, reversed the suppressive influence of DLX2-AS1 overexpression on the inflammatory response and apoptosis of PDLCs. CONCLUSIONS: DLX2-AS1 restrains inflammatory response and apoptosis of PDLCs via the microRNA-330-3p/RO60 axis.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
MicroRNAs
/
RNA Longo não Codificante
Idioma:
En
Revista:
Arch Oral Biol
Ano de publicação:
2022
Tipo de documento:
Article
País de afiliação:
China