LncRNA Miat promotes neuropathic pain through miR-362-3p/BAMBI signaling axis.
Exp Cell Res
; 420(2): 113359, 2022 11 15.
Article
en En
| MEDLINE
| ID: mdl-36122770
ABSTRACT
The treatment of neuropathic pain (NP) has become an important subject to be studied and solved urgently in clinical practice. The role of long noncoding RNAs (lncRNAs) in NP development is becoming clear. Therefore, this study aimed to investigate the role and mechanism of lncRNA Miat in NP. In this study, chronic contractionary injury (CCI) mouse NP model was performed. Firstly, the effects of Miat on pain behavior in mice and the expression levels of pro-inflammatory cytokines and pro-inflammatory proteins in spinal cord tissue were explored by interfering with the expression of Miat. Then, Miat-targeted signaling pathway was predicted by bioinformatics and verified by dual luciferase reporter gene and RNA pull down. Finally, the mechanism of Miat was confirmed by the rescue experiments. Our results demonstrated that Miat knockdown alleviated paw withdrawal threshold, paw withdrawal latency, cold hyperalgesia frequency and neuroinflammation in CCI mice. MiR-362-3p was able to bind to Miat and BAMBI. Overall, Miat upregulated BAMBI by inhibiting miR-362-3p, thereby promoting the occurrence and development of NP. This study analyzed the possibility and effectiveness of targeting Miat for NP clinical treatment, in order to provide new ideas and technical methods for NP gene therapy.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
MicroARNs
/
ARN Largo no Codificante
/
Neuralgia
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Exp Cell Res
Año:
2022
Tipo del documento:
Article
País de afiliación:
China