ArticleThe Journal of biological chemistry2015
Increased NF-κB Activity and Decreased Wnt/β-Catenin Signaling Mediate Reduced Osteoblast Differentiation and Function in ΔF508 Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Mice.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 45 citations in OpenAlex.
- Targeting Elastin-Derived Peptides Reverses Alveolar Epithelial Dysfunction in Chronic Obstructive Pulmonary Disease.MedComm · 2026Article
- CFTR mediates ClNature communications · 2026Article
- Adverse effects of vanzacaftor-tezacaftor-deutivacaftor in a cystic fibrosis population: A case series.Respiratory medicine case reports · 2026Article
- Bone Disease in Cystic Fibrosis: Insights into Etiopathogenesis and Advances in Treatment Management.Journal of clinical medicine · 2025Review
- CFTR mutation is associated with bone differentiation abnormalities in cystic fibrosis.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2025Article
- Interleukin 26 attenuates osteoblast differentiation in osteoarthritis patients by activating COX2 and NF-κB pathways.International journal of medical sciences · 2025Article
- Cystic Fibrosis Bone Disease: The Interplay between CFTR Dysfunction and Chronic Inflammation.Biomolecules · 2023Review
- CFTR and Gastrointestinal Cancers: An Update.Journal of personalized medicine · 2022Review
- Systemic bis-phosphinic acid derivative restores chloride transport in Cystic Fibrosis mice.Scientific reports · 2022Article
- Magnesium implantation or supplementation ameliorates bone disorder in CFTR-mutant mice through an ATF4-dependent Wnt/β-catenin signaling.Bioactive materials · 2022Article
- Role of inflammation and oxidative stress in tissue damage associated with cystic fibrosis: CAPE as a future therapeutic strategy.Molecular and cellular biochemistry · 2022Review
- Semaphorin3A promotes osseointegration of titanium implants in osteoporotic rabbits.Clinical oral investigations · 2022Article
- Interaction of NF-κB and Wnt/β-catenin Signaling Pathways in Alzheimer's Disease and Potential Active Drug Treatments.Neurochemical research · 2021Review
- [Cystic fibrosis being a polyendocrine disease (Review)].Problemy endokrinologii · 2021Review
- Prognosis-Based Early Intervention Strategies to Resolve Exacerbation and Progressive Lung Function Decline in Cystic Fibrosis.Journal of personalized medicine · 2021Article
- Bone Cells Differentiation: How CFTR Mutations May Rule the Game of Stem Cells Commitment?Frontiers in cell and developmental biology · 2021Review
- Quercetin as an Agent for Protecting the Bone: A Review of the Current Evidence.International journal of molecular sciences · 2020Review
- Review
- Article
- JZL184, A Monoacylglycerol Lipase Inhibitor, Induces Bone Loss in a Multiple Myeloma Model of Immunocompetent Mice.Calcified tissue international · 2020Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The prevalent human ΔF508 mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) is associated with reduced bone formation and bone loss in mice. The molecular mechanisms by which the ΔF508-CFTR mutation causes alterations in bone formation are poorly known. In this study, we analyzed the osteoblast phenotype in ΔF508-CFTR mice and characterized the signaling mechanisms underlying this phenotype. Ex vivo studies showed that the ΔF508-CFTR mutation negatively impacted the differentiation of bone marrow stromal cells into osteoblasts and the activity of osteoblasts, demonstrating that the ΔF508-CFTR mutation alters both osteoblast differentiation and function. Treatment with a CFTR corrector rescued the abnormal collagen gene expression in ΔF508-CFTR osteoblasts. Mechanistic analysis revealed that NF-κB signaling and transcriptional activity were increased in mutant osteoblasts. Functional studies showed that the activation of NF-κB transcriptional activity in mutant osteoblasts resulted in increased β-catenin phosphorylation, reduced osteoblast β-catenin expression, and altered expression of Wnt/β-catenin target genes. Pharmacological inhibition of NF-κB activity or activation of canonical Wnt signaling rescued Wnt target gene expression and corrected osteoblast differentiation and function in bone marrow stromal cells and osteoblasts from ΔF508-CFTR mice. Overall, the results show that the ΔF508-CFTR mutation impairs osteoblast differentiation and function as a result of overactive NF-κB and reduced Wnt/β-catenin signaling. Moreover, the data indicate that pharmacological inhibition of NF-κB or activation of Wnt/β-catenin signaling can rescue the abnormal osteoblast differentiation and function induced by the prevalent ΔF508-CFTR mutation, suggesting novel therapeutic strategies to correct the osteoblast dysfunctions in cystic fibrosis.
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