ArticleExperimental and therapeutic medicine2018
TGF-β1 stimulates epithelial-mesenchymal transition mediated by ADAM33.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- ADAM33 Silencing Inhibits Vascular Smooth Muscle Cell Migration and Regulates Cytokine Secretion in Airway Vascular Remodeling via the PI3K/AKT/mTOR Pathway.Canadian respiratory journal · 2022Article
- Silencing a disintegrin and metalloproteinase‑33 attenuates the proliferation of vascular smooth muscle cells via PI3K/AKT pathway: Implications in the pathogenesis of airway vascular remodeling.Molecular medicine reports · 2021Article
- Syndecan-1 Amplifies Ovalbumin-Induced Airway Remodeling by Strengthening TGFβ1/Smad3 Action.Frontiers in immunology · 2021Article
- MiR-203a-3p regulates TGF-β1-induced epithelial-mesenchymal transition (EMT) in asthma by regulating Smad3 pathway through SIX1.Bioscience reports · 2020Article
- Human cytomegalovirus infection enhances invasiveness and migration of glioblastoma cells by epithelial-to-mesenchymal transition.International journal of clinical and experimental pathology · 2020Article
- Epithelial mesenchymal transition (EMT): a universal process in lung diseases with implications for cystic fibrosis pathophysiology.Respiratory research · 2018Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to determine the effects of transforming growth factor (TGF)-β1 on disintegrin and metalloproteinase domain-containing protein 33 (ADAM33) expression in airway epithelial cells in order to investigate the association between ADAM33 expression and TGF-β1-induced epithelial to mesenchymal transition (EMT), and to further explore the mechanisms underlying the role of ADAM33 in airway remodeling in asthma. The human bronchial epithelial cell line HBE was transfected with small interfering RNA targeting ADAM33 (siADAM33) and treated with different concentrations of TGF-β1 (10, 20 or 30 ng/ml), while untransfected cells were used as controls. At 72 h after treatment, cellular morphology and immunohistochemical staining were observed under a microscope. The protein and mRNA expression levels of ADAM33 and the EMT markers E-cadherin and vimentin were detected by western blot analysis and reverse-transcription quantitative polymerase chain reaction, respectively. In addition, a correlation analysis of ADAM33 expression and E-cadherin/vimentin expression was performed. A wound healing migration assay and a cell invasion assay were also performed. The results of the cellular morphology, migration and invasion studies suggested that TGF-β1 treatment induced typical EMT changes in HBE cells. In addition, treatment with various concentrations of TGF-β1 significantly increased the protein and mRNA expression levels of ADAM33 and vimentin compared with those in untreated cells. TGF-β1 treatment also decreased the protein and mRNA expression levels of E-cadherin in a dose-dependent manner. By contrast, transfection with siADAM33 promoted the protein expression of E-cadherin and decreased the protein expression of vimentin. Furthermore, ADAM33 and E-cadherin expression levels exhibited a significant negative correlation, whereas ADAM33 and vimentin were positively correlated. In conclusion, the results suggested that TGF-β1 enhances ADAM33 expression in airway epithelial cells, and that ADAM33 induces the EMT of airway epithelial cells, thus participating in airway remodeling in asthma.
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