STOML2 Knockdown Inhibits Inflammation and Airway Remodeling of PDGF-BB-Induced Airway Smooth-Muscle Cells by the MAPK Pathway.

Asthma is a chronic inflammatory airway disease characterized by airway inflammation and remodeling. Abnormal proliferation and migration of human airway smooth muscle cells (HASMCs), induced by platelet-derived growth factor BB (PDGF-BB), are associated with the occurrence and progression of asthma. In this study, we aim to investigate the expression and molecular mechanisms of STOML2 in airway remodeling in asthma. PDGF-BB-stimulated HASMCs were used as the asthma cell model. STOML2 expression levels in the serum of patients with asthma and healthy controls were measured using qRT-PCR. Additionally, qRT-PCR and western blotting were used to measure STOML2, E-cadherin, and N-cadherin expression in HASMCs. Extracellular matrix components were detected by western blot assay. The viability and migration of HASMCs were analyzed using MTT and Transwell assays. Tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and IL-6 contents were evaluated using the corresponding kits. The key molecules of the p38 MAPK pathway (p38 and p38) were determined using western blotting. Increased STOML2 expression was observed in both patients with asthma and PDGF-BB-treated HASMCs. STOML2 knockdown inhibits STOML2 expression in HASMCs. PDGF-BB induced proliferation, migration, extracellular matrix deposition, inflammatory responses, and p38 MAPK pathway activation in HASMCs. However, the opposite effects were observed following STOML2 knockdown or SB-203580 treatment, respectively. Furthermore, P79350 treatment reversed the effect of STOML2 knockdown. our results showed that silencing STOML2 inhibits inflammation and airway remodeling in PDGF-BB-stimulated HASMCs via the p38 MAPK pathway. Thus, STOML2 is a promising therapeutic target for the treatment of asthma.