ArticleThe Kaohsiung journal of medical sciences2020
TNFSF14, a novel target of miR-326, facilitates airway remodeling in airway smooth muscle cells via inducing extracellular matrix protein deposition and proliferation.
Article in The Kaohsiung journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Qufeng Jiejing formula ameliorated the injury of airway smooth muscle cells induced by platelet-derived growth factor-BB through the transforming growth factor-β1/Smads signaling pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Serum miR-130a-3p and miR-326: Correlation with Airway Inflammation and Prognostic Implications in Pediatric Bronchial Asthma.Journal of asthma and allergy · 2025Article
- MiR-326-mediated overexpression of NFIB offsets TGF-β induced epithelial to mesenchymal transition and reverses lung fibrosis.Cellular and molecular life sciences : CMLS · 2023Article
- Noncoding RNAs in asthmatic airway smooth muscle cells.European respiratory review : an official journal of the European Respiratory Society · 2023Review
- Semaphorin 7a aggravates TGF-β1-induced airway EMT through the FAK/ERK1/2 signaling pathway in asthma.Frontiers in immunology · 2023Article
- Long noncoding RNA ANRIL up-regulates CCND1 via sponging miR-98-5p to promote TGF-β1-induced human airway smooth muscle cell proliferation, migration, and extracellular matrix deposition.The Kaohsiung journal of medical sciences · 2022Article
- Article
- Syndecan-1 Amplifies Ovalbumin-Induced Airway Remodeling by Strengthening TGFβ1/Smad3 Action.Frontiers in immunology · 2021Article
- TNFSF14, a novel target of miR-326, facilitates airway remodeling in airway smooth muscle cells via inducing extracellular matrix protein deposition and proliferation.The Kaohsiung journal of medical sciences · 2020Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a common chronic respiratory disease, the incidence of asthma is increasing in recent years worldwide. Airway remodeling is the primary pathological basis of refractory asthma, but the studies about the underlying mechanism of airway remodeling was a lack. In the study, we aimed to investigate the effects and mechanisms of miR-326 on airway remodeling in airway smooth muscle cells (ASMCs). The results showed that transforming growth factor-β1 (TGF-β1) accelerated matrix protein deposition by increasing the expression levels of collagen I and fibronectin, and promoted proliferative ability of ASMCs. However, miR-326 was significantly downregulated in TGF-β1-treated ASMCs. MiR-326 mimics robustly decreased the collagen I and fibronectin levels and inhibited cell proliferation of TGF-β1-treated ASMCs. Luciferase assay investigated that tumor necrosis factor superfamily member 14 (TNFSF14) was a direct target of miR-326. The expression of TNFSF14 was negatively regulated by miR-326. Moreover, exogenous TNFSF14 effectively reversed the inhibitory effects of miR-326 overexpression on the expression levels of collagen I and fibronectin, and promoted cell proliferation of TGF-β1-treated ASMCs. In conclusion, miR-326 suppressed matrix protein deposition and cell proliferation of TGF-β1-treated ASMCs via inhibiting TNFSF14. MiR-326 might be a promising novel therapeutic target for asthma.
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