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Published on: October 30, 2019
TRIM37 inhibits PDGF-BB-induced proliferation and migration of airway smooth muscle cells
Ying Dai1, Ying Li1, Ruiduo Cheng1
1Department of Pediatrics, Henan University Huaihe Hospital, Kaifeng, 475000, Henan Province, PR China.
Abstract:
Tripartite motif 37 (TRIM37) belongs to the TRIM family of proteins and has been reported to be involved in the progression of asthma. However, the effects of TRIM37 on airway smooth muscle cells (ASMCs) proliferation and migration are still unknown. This study aimed to investigate the effects of TRIM37 on cell proliferation and migration in platelet-derived growth factor BB (PDGF-BB)-stimulated ASMCs, and the potential molecular mechanisms was also explored. Our data demonstrated that the expression of TRIM37 was significantly decreased in ASMCs stimulated with PDGF-BB. In addition, overexpression of TRIM37 efficiently suppressed PDGF-BB-induced ASMCs proliferation and migration. Furthermore, overexpression of TRIM37 obviously inhibited the protein expression levels of β-catenin, c-Myc and cyclinD1 in PDGF-BB-stimulated ASMCs. The Wnt/β-catenin pathway activator LiCl significantly reversed the inhibitory effects of TRIM37 on cell proliferation and migration in PDGF-BB-stimulated ASMCs. Taken together, these results demonstrate that TRIM37 inhibits the proliferation and invasion of ASMCs cultured with PDGF-BB through suppressing the Wnt/β-catenin signaling pathway.
Insights
Tripartite motif 37 (TRIM37) suppresses airway smooth muscle cell proliferation and migration. This protein inhibits the Wnt/β-catenin pathway, offering potential therapeutic targets for asthma.
Area of Science:
- Cell Biology
- Molecular Biology
- Respiratory Medicine
Background:
- Tripartite motif 37 (TRIM37) is a TRIM family protein implicated in asthma.
- The role of TRIM37 in airway smooth muscle cell (ASMC) proliferation and migration remains unclear.
Purpose of the Study:
- To investigate the effect of TRIM37 on platelet-derived growth factor BB (PDGF-BB)-stimulated ASMC proliferation and migration.
- To explore the underlying molecular mechanisms of TRIM37 action.
Main Methods:
- ASMCs were stimulated with PDGF-BB.
- TRIM37 expression was manipulated (overexpressed).
- Cell proliferation and migration assays were performed.
- Western blotting analyzed protein expression (β-catenin, c-Myc, cyclinD1).
- Wnt/β-catenin pathway activation was induced using LiCl.
Main Results:
- PDGF-BB stimulation decreased endogenous TRIM37 expression in ASMCs.
- TRIM37 overexpression inhibited PDGF-BB-induced ASMC proliferation and migration.
- TRIM37 overexpression suppressed β-catenin, c-Myc, and cyclinD1 protein levels.
- LiCl treatment reversed the inhibitory effects of TRIM37.
Conclusions:
- TRIM37 inhibits ASMC proliferation and migration induced by PDGF-BB.
- TRIM37 exerts its inhibitory effects by suppressing the Wnt/β-catenin signaling pathway.
- TRIM37 represents a potential therapeutic target for asthma-related airway remodeling.
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