RAB11A aggravates PDGF-BB-stimulated proliferation, migration, and inflammation of airway smooth muscle cells via affecting the NF-kB and PI3K/AKT pathways
Artículo
en Inglés
| IBECS (España) | ID: ibc-208906
Background:
Pediatric asthma is an usual disease and a kind of fearful health threat for chil-dren. Airwaysmooth muscle cells (ASMCs) with increased cell proliferation and migration abil-ities serve as important features in the progression of asthma. RAB11A has been shown to aggravate cancer progression and is closely associated with inflammation. Geneanalysis dis-covered that RAB11A exhibited higher expression in asthmatic patients. However, the detailed regulatory function of RAB11A in asthma still needs further investigation.
In this study, the mRNA and protein expressions of RAB11A were increased with PDGF-BBtreatment in a dose-dependent manner. Additionally, the silencing of RAB11A sup-pressed the proliferation ability of PDGF-BB-mediated ASMCs. Moreover, it was uncovered that the knockdown of RAB11A inhibited the migration ability of PDGF-BB-stimulated ASMCs. Besides, suppression of RAB11A relieved the inflammatory response in PDGF-BB-stimulated ASMCs. Lastly, inhibition of RAB11A retarded the NF-κB and PI3K/AKT pathways.
Conclusion:
Our results revealed that RAB11A aggravated PDGF-BB-stimulated proliferation, migration, and inflammation of ASMCs through modulating NF-κB and PI3K/AKT signaling path-ways. This finding implied that the RAB11A may be deemed as a novel and prospective bio-marker for asthmatreatment (AU)