Therapeutic potential of proteasome inhibitors for dihydropyridine‐induced gingival overgrowth

Objectives NF‐κB plays a crucial role in collagen overproduction in dihydropyridine‐induced gingival overgrowth (DIGO) fibroblasts. We aim to investigate the role of the kappa B (IκB) kinase (IKK)–NF‐κB pathway and downstream collagen type I (Col I) synthesis in DIGO cells and to demonstrate the the...

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Bibliographic Details
Published in:Oral diseases 2020-04, Vol.26 (3), p.630-636
Main Authors: Lu, Sao‐Lun, Chang, Jui‐Hung, Huang, Chiung‐Fang, Chen, Li‐Sheng
Format: Article
Language:English
Subjects:
Bortezomib
canonical NF‐κB pathway
collagen type I
Cytosol
Dentistry
Dihydropyridine
Fibroblasts
Gingiva
IKK protein
IL‐1β
Inflammation
Nifedipine
Nuclear transport
Phosphorylation
proteasome inhibitor
Proteasome inhibitors
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Summary:Objectives NF‐κB plays a crucial role in collagen overproduction in dihydropyridine‐induced gingival overgrowth (DIGO) fibroblasts. We aim to investigate the role of the kappa B (IκB) kinase (IKK)–NF‐κB pathway and downstream collagen type I (Col I) synthesis in DIGO cells and to demonstrate the therapeutic strategy of interference of this pathway with proteasome inhibitors. Methods Gingival fibroblasts from DIGO (n = 5) and healthy (n = 5) patients were selected and stimulated with IL‐1β, nifedipine, or both. All experiments were run in triplicate and independently for each primary cell sample. Results The results demonstrated that both drugs additively mediated NF‐κB activity by activating IKKα/β phosphorylation. They also triggered nuclear translocation of NF‐κB, Rela, and p50 (*p 
ISSN:1354-523X
1601-0825
DOI:10.1111/odi.13260