Vibration activates the actin/NF-κB axis and upregulates IL-6 and IL-8 expression in human periodontal ligament cells.


Journal

Cell biology international
ISSN: 1095-8355
Titre abrégé: Cell Biol Int
Pays: England
ID NLM: 9307129

Informations de publication

Date de publication:
Feb 2020
Historique:
received: 25 05 2019
accepted: 23 11 2019
pubmed: 27 11 2019
medline: 30 9 2020
entrez: 27 11 2019
Statut: ppublish

Résumé

We previously reported that mechanical vibration-induced proinflammatory cytokines, interleukin-6 (IL-6) and IL-8, expression in human periodontal ligament (hPDL) cells, however, the underlying mechanism remained unclear. Mechanical stimuli are able to activate cellular responses by inducing the activation of several signaling pathways including cytoskeletal changes and inflammation. The actin cytoskeleton is a highly dynamic network and plays many important roles in intracellular events. Here, we aimed to investigate the involvement of a pivotal mediator of inflammatory responses, nuclear factor-κB (NF-κB), and actin polymerization in vibration-induced upregulation of IL-6 and IL-8 expression in hPDL cells. hPDL cells were pretreated with the NF-κB inhibitor BAY 11-7082 or cytochalasin D, respectively, before exposure to vibration. IL-6 and IL-8 messenger RNA (mRNA) and protein expression were quantified by quantitative polymerase chain reaction and enzyme-linked immunosorbent assays, respectively. Subcellular localization of the NF-κB p65 subunit was visualized by immunofluorescent staining. We found an increase in NF-κB nuclear translocation in vibrated cells compared with control cells. Pretreatment with BAY 11-7082 significantly inhibited vibration-induced IL-6 and IL-8 mRNA and protein expression in hPDL cells. Moreover, pretreatment with cytochalasin D inhibited NF-κB nuclear translocation and attenuated upregulation of IL-6 and IL-8 mRNA and protein in vibrated cells. Therefore, modulation of actin cytoskeletal polymerization in response to vibration may activate the NF-κB signaling pathway and subsequently upregulate IL-6 and IL-8 expression in hPDL cells.

Identifiants

pubmed: 31769560
doi: 10.1002/cbin.11267
doi:

Substances chimiques

Actins 0
CXCL8 protein, human 0
IL6 protein, human 0
Interleukin-6 0
Interleukin-8 0
NF-kappa B 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

661-670

Subventions

Organisme : Research funding, Faculty of Dentistry, Prince of Songkla University

Informations de copyright

© 2019 International Federation for Cell Biology.

Références

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Auteurs

Pussadee Phusuntornsakul (P)

Trang Hospital, Muang, Trang, 92000, Thailand.

Suwanna Jitpukdeebodintra (S)

Department of Oral Biology, Faculty of Dentistry, Prince of Songkla University, Hat Yai, Songkhla, 90110, Thailand.

Prasit Pavasant (P)

Department of Anatomy, Faculty of Dentistry, Chulalongkorn University, Bangkok, 10330, Thailand.

Chidchanok Leethanakul (C)

Department of Preventive Dentistry, Orthodontic Section, Oral Neuroscience and Molecular Biology of Dental Pulp and Bone Cells Research Unit, Faculty of Dentistry, Prince of Songkla University, Hat Yai, Songkhla, 90110, Thailand.

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