ArticleRespiratory research2017
Effect of active vitamin D3 on VEGF-induced ADAM33 expression and proliferation in human airway smooth muscle cells: implications for asthma treatment.
Article in Respiratory research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- The Role of Vitamin D Supplementation on Airway Remodeling in Asthma: A Systematic Review.Nutrients · 2023Pooled it
- Article
- Vitamin D3 suppresses NLRP3 inflammasome pathway and enhances steroid sensitivity in a neutrophilic steroid hyporesponsive asthma mouse model.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Impact of vitamin D on hyperoxic acute lung injury in neonatal mice.BMC pulmonary medicine · 2024Article
- Vitamin D and allergic diseases.Frontiers in immunology · 2024Review
- Vascular endothelial growth factor induces the migration of human airway smooth muscle cells by activating the RhoA/ROCK pathway.BMC pulmonary medicine · 2023Article
- Role of ADAM and ADAMTS proteases in pathological tissue remodeling.Cell death discovery · 2023Review
- Induction of heme oxygenase-1 antagonizes PM2.5-induced pulmonary VEGFA expression through regulating HIF-1α.Journal of biochemical and molecular toxicology · 2023Article
- Polymorphism in ADAM33 gene associated with asthmatics in West Bengal, India - An investigation by in-silico analysis.The World Allergy Organization journal · 2023Article
- Review
- Does Vitamin D Work Synergistically with Anti-Asthmatic Drugs in Airway Remodeling?International journal of molecular sciences · 2022Article
- Vitamin DFrontiers in pharmacology · 2022Article
- Pathobiology of Airway Remodeling in Asthma: The Emerging Role of Integrins.Journal of asthma and allergy · 2022Review
- ADAM and ADAMTS disintegrin and metalloproteinases as major factors and molecular targets in vascular malfunction and disease.Advances in pharmacology (San Diego, Calif.) · 2022Article
- Article
- The strong correlation between ADAM33 expression and airway inflammation in chronic obstructive pulmonary disease and candidate for biomarker and treatment of COPD.Scientific reports · 2021Article
- 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
- A Disintegrin and Metalloproteinase (ADAM) and ADAM with thrombospondin motifs (ADAMTS) family in vascular biology and disease.Biochemical pharmacology · 2019Review
- Mechanisms shaping the role of ERK1/2 in cellular senescence (Review).Molecular medicine reports · 2019Review
- Effect of simvastatin on expression of VEGF and TGF-β1 in atherosclerotic animal model of type 2 diabetes mellitus.Experimental and therapeutic medicine · 2018Article
Corrections and comments
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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
backgroundAsthma is a chronic respiratory disease characterized by reversible airway obstruction with persistent airway inflammation and airway remodeling, which is associated with increased airway smooth muscle (ASM) mass. Vascular endothelial growth factor (VEGF) has been implicated in inflammatory and airway blood vessel remodeling in asthma. Recent evidence indicates that a deficiency of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) may influence asthma pathogenesis. A disintegrin and metalloproteinase (ADAM)33 has been identified as playing a role in the pathophysiology of asthma. ADAM33, which is expressed in ASM cells, is suggested to play a role in the function of these cells. Recent studies show that 1,25-(OH)2D3 exerts direct inhibitory effects on passively sensitized human ASM cells in vitro, including inhibition of ADAM33 expression and cell proliferation; however, the mechanism has not been fully understood.
methodsIn order to elucidate the precise mechanism underlying the effect of 1,25(OH)2D3 on VEGF-induced ADAM33 expression and ASM cell proliferation, we tested the effects of 1,25(OH)2D3 on cell cycle progression and evaluated the levels of phospho-VEGF receptor 2 (VEGFR2), phospho-extracellular signal-regulated kinase 1/2 (ERK1/2), and phospho-Akt in VEGF-stimulated ASM cells.
resultsWe found that 1,25(OH)2D3 inhibited VEGF-induced ADAM33 expression and ASM cell proliferation, as well as cell cycle arrest. Additionally, VEGF-induced ADAM33 expression and ASM cell proliferation was suppressed via inhibition of ERK1/2 activity, but not that of Akt. Furthermore, 1,25(OH)2D3 treatment inhibited VEGF-induced activation of VEGFR2 as well as that of ERK and Akt in a concentration-dependent manner. 1,25(OH)2D3 also inhibited transforming growth factor (TGF)-β-induced VEGF secretion by ASM cells.
conclusionsCollectively, our findings suggest that 1,25(OH)2D3 inhibits VEGF-induced ASM cell proliferation by suppressing VEGFR2 and ERK1/2 activation and downregulating ADAM33. Further studies of these mechanisms are needed to facilitate the development of treatments for smooth muscle hyperplasia-associated diseases of the airway such as asthma.
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