miR1865p regulates the inflammatory response of chronic obstructive pulmonary disorder by targeting HIF1α.
Mol Med Rep
; 29(2)2024 02.
Article
em En
| MEDLINE
| ID: mdl-38214374
ABSTRACT
Chronic obstructive pulmonary disorder (COPD) is a chronic respiratory disease that is a major cause of morbidity and mortality worldwide. Previous studies have shown that miR1865p expression is significantly increased in COPD and is involved in multiple physiological and pathological processes. However, the role of miRNA1865p in the inflammatory response of COPD remains unclear. In this study, an in vitro model of COPD was established using lipopolysaccharide (LPS)induced human bronchial epithelial cells (BEAS2B). CCK8 assays, flow cytometry, and a Muse cell analyzer were used to determine cell viability, cell cycle distribution, and apoptosis, respectively. The production of TNFα and IL6 were measured by ELISA. Reversetranscriptionquantitative PCR and western blotting were used to analyze mRNA and protein expression levels. The targeting relation between miR1865p and HIF1α was discovered using dualluciferase reporter assays. The results showed that transfection of miR1865p inhibitor inhibited cell proliferation and promoted cell apoptosis in the LPSinduced BEAS2B cells. Inhibition of miR1865p markedly increased the levels of TNFα and IL6. miR1865p directly targeted and negatively regulated HIF1α expression. In addition, inhibition of miR1865p increased the expression of the NFκB pathway protein pp65. In conclusion, it was found that inhibiting miR1865p may improve inflammation of COPD through HIF1α in LPSinduced BEAS2B cells, possibly by regulating NFκB signaling. These findings provide a novel potential avenue for the clinical management of COPD. Future research is required to determine the mechanism of the interaction between miR1865p and HIF1α in COPD.
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Base de dados:
MEDLINE
Assunto principal:
Doença Pulmonar Obstrutiva Crônica
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MicroRNAs
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article