Back to Search
Start Over
TWEAK/Fn14 interaction induces proliferation and migration in human airway smooth muscle cells via activating the NF‐κB pathway
- Source :
- Journal of Cellular Biochemistry. 119:3528-3536
- Publication Year :
- 2018
- Publisher :
- Wiley, 2018.
-
Abstract
- Asthma, an increasingly common chronic disease among children, are characterized by airway remodeling, which is partly attributed to the proliferation and migration of airway smooth muscle cell (ASMC). The purpose of the present study was to investigate potential roles and mechanisms of the tumor necrosis factor-like weak inducer of apoptosis (TWEAK)/fibroblast growth factor-inducible molecule 14 (Fn14) axis on cell proliferation and migration in HASMCs. Compared to HASMCs from non-asthmatic patients, those from asthmatic patients showed elevated expression levels of both Fn14 and TWEAK. Additionally, similar to the response triggered by platelet-derived growth factor-BB, stimulation with recombinant TWEAK strongly induced cell proliferation and migration in HASMCs. However, depletion of Fn14 remarkably abrogated the enhancement of TWEAK on the cell proliferation and migration of HASMCs. Furthermore, treatment with TWEAK led to the activation of NF-κB. This effect was eliminated by silencing Fn14, indicating that TWEAK-induced NF-κB signaling was mediated via Fn14. Moreover, the TWEAK/Fn14 interaction promoted cell proliferation and migration. These effects were blocked by NF-κB inhibitor SN50, which suggest that the TWEAK/Fn14 signaling system partially depends on NF-κB activity. Collectively, we demonstrated that the TWEAK/Fn14 axis accelerated HASMC cell proliferation and migration by activating the NF-κB pathway, thereby exacerbating airway remodeling in asthma. Altogether, these findings indicate a novel role for the TWEAK/Fn14/NF-κB pathway as a potent option for limiting airway remodeling in asthma.
- Subjects :
- 0301 basic medicine
Blotting, Western
Myocytes, Smooth Muscle
Stimulation
Biology
Biochemistry
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Cell Movement
medicine
Humans
Gene silencing
Inducer
Fibroblast
Molecular Biology
Cells, Cultured
Cell Proliferation
Wound Healing
Reverse Transcriptase Polymerase Chain Reaction
Cell growth
NF-kappa B
Cytokine TWEAK
NF-κB
Cell Biology
Asthma
Cell biology
030104 developmental biology
medicine.anatomical_structure
030228 respiratory system
chemistry
TWEAK Receptor
Apoptosis
Immunology
Tumor necrosis factor alpha
Protein Binding
Signal Transduction
Subjects
Details
- ISSN :
- 10974644 and 07302312
- Volume :
- 119
- Database :
- OpenAIRE
- Journal :
- Journal of Cellular Biochemistry
- Accession number :
- edsair.doi.dedup.....747b505765884d400760135b9f9e9ea5
- Full Text :
- https://doi.org/10.1002/jcb.26525