TRIM33 Modulates Inflammation and Airway Remodeling of PDGF-BB-Induced Airway Smooth-Muscle Cells by the Wnt/ β-Catenin Pathway

In this study, the TRIM33 expressions in serum samples and platelet-derived growth factor BB (PDGF-BB)-induced airway smooth-muscle cells (ASMCs) were evaluated. A gain-of-function experiment was performed, and cell proliferation and migration were detected using CCK-8 and w ound healing assays. Besides, the protein levels of EMT biomarkers and airway-remodeling markers were determined by Western blot assay. ELISA analyzed the contents of IL-1β, IL-6, and TNF-α in the supernatant. The modulation of Smad4 expression and subsequent activation of Wnt/β-catenin by TRIM33 were also assessed. We found that TRIM33 was downregulated in the serum from children who were asthma patients and PDGF-BB-induced ASMCs. TRIM33 overexpression showed decrease of PDGF-BB-induced ASMC proliferation and migration. Moreover, the augment of TRIM33 reduced the PDGF-BB-induced cell EMT a nd airway-remodeling marker levels and suppressed the secretions of inflammatory cytokines in PDGF-BB-induced ASMCs. Additionally, TRIM33 overexpression inhibited activation of Wnt/β-catenin via reducing Smad4 expression to regulate asthma inflammation and airway remodeling. All in all, our study r evealed that TRIM33 expression was downregulated in children who were asthma patients and PDGF-BB-induced ASMCs. TRIM33 modulated PDGF-BB-induced inflammation and airway remodeling of ASMCs by the Wnt/β-catenin pathway via regulating Smad4, which may provide a new treatment direction for asthma.Int Arch Allergy Immunol
Source: International Archives of Allergy and Immunology - Category: Allergy & Immunology Source Type: research