STOML2 Suppresses the Proliferation, Migration, and Inflammation of Airway Smooth Muscle Cells in Children with Asthma by Inhibiting NLRP3

Abstract

Background: Asthma is a chronic disease of the airways which involves airway remodeling and inflammation. Stomatin like protein-2 (STOML2) regulates immunity and inflammation. This study aimed to elucidate the functional role of STOML2 in childhood asthma and the mechanisms by which it acts. Materials and Methods: Airway smooth muscle cells (ASMCs) treated with platelet-derived growth factor-BB (PDGF-BB) were used to mimic airway hyper-reactivity in vitro. STOML2 expression in serum from patients with asthma and in PDGF-BB-induced ASMCs was evaluated by quantitative real-time PCR (qRT-PCR) and western blot assays. Cell proliferation was detected by cell counting kit-8 (CCK-8) and colony formation assays. Cell migration and invasion were measured by wound healing and transwell assays. Enzyme-linked immunosorbent assay (ELISA) was applied to analyze the expression of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) in PDGF-BB-induced ASMCs. The levels of the nucleotide-binding oligomerization domain-like receptor (NLR) containing pyrin domain 3 (NLRP3) inflammasome were assessed by western blot assay. Results: STOML2 was decreased in the serum of children with asthma and in PDGF-BB-induced ASMCs (p < 0.01). Overexpression of STOML2 reduced the proliferation, migration, and invasion of PDGF-BB-induced ASMCs (p < 0.01). Increased STOML2 suppressed the secretion of inflammatory cytokines in PDGF-BB-induced ASMCs (p < 0.05). In addition, STOML2 overexpression inhibited the activation of the NLRP3 inflammasome. Conclusions: STOML2 regulated the inflammation and airway remodeling of ASMCs induced by PDGF-BB through inhibiting NLRP3, which might provide a novel direction for the treatment of asthma.