SNP rs322931 (C>T) in miR-181b and rs7158663 (G>A) in MEG3 aggravate the inflammatory response of anal abscess in patients with Crohn's disease.
Aging (Albany NY)
; 14(7): 3313-3324, 2022 04 14.
Article
em En
| MEDLINE
| ID: mdl-35422450
ABSTRACT
BACKGROUND:
The MEG3/miR-181b signaling has been implicated in the pathogenesis of several diseases including Crohn's disease. This work aimed to study the correlation between SNPs in MEG3/miR-181b and the severity of anal abscess in patients with Crohn's disease.METHODS:
Quantitative real-time PCR was performed to analyze the expression of MEG3 and miR-181b. ELISA was carried out to examine the expression of TNF-α, IL-1ß, IL-6, CRP, SSA, AAT, AAG and HPT in the peripheral blood of patients with Crohn's disease. Luciferase assay was performed to explore the role of miR-181b in the expression of MEG3 and TNF-α.RESULTS:
The expression of MEG3 and miR-181b in the peripheral blood of patients with Crohn's disease was remarkably associated with the rs322931 and rs7158663 polymorphisms. rs322931 (C>T) in miR-181b and rs7158663 (G>A) in MEG3 significantly promoted the expression of TNF-α, IL-1ß, IL-6, CRP, SSA, AAT, AAG and HPT. Luciferase assay demonstrated that miR-181b was capable of repressing the expression of MEG3 and TNF-α through binding to their specific binding sites. Moreover, alteration of MEG3 and miR-181b expression also showed a remarkable impact on the MEG3/miR-181b/TNF-α signaling pathway in THP-1 cells.CONCLUSIONS:
In conclusion, our study demonstrated that two SNPs, rs322931 (C>T) in miR-181b and rs7158663 (G>A) in MEG3, could aggravate the inflammatory response of anal abscess in patients with Crohn's disease via modulating the MEG3/miR-181b/TNF-α signaling pathway.Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Doenças do Ânus
/
Doença de Crohn
/
MicroRNAs
/
Abscesso
/
RNA Longo não Codificante
Limite:
Humans
Idioma:
En
Revista:
Aging (Albany NY)
Assunto da revista:
GERIATRIA
Ano de publicação:
2022
Tipo de documento:
Article
País de afiliação:
China