[S] TRPA1 up‐regulation mediates oxidative stress in a pulpitis model in vitro

A tétel rövid nézete
dc.contributor.authorKunka, Árpád
dc.contributor.authorLisztes, Erika
dc.contributor.authorBohács, Judit
dc.contributor.authorRacskó, Márk
dc.contributor.authorKelemen, Balázs
dc.contributor.authorKovalecz, Gabriella
dc.contributor.authorTóth, Etelka D.
dc.contributor.authorHegedűs, Csaba
dc.contributor.authorBágyi, Kinga
dc.contributor.authorMarincsák, Rita
dc.contributor.authorTóth, Balázs István
dc.contributor.authorKunka Árpád (2024-) (xxx)
dc.contributor.authorLisztes Erika (2024-) (xxx)
dc.contributor.authorBohács Judit (1993-) (Fogorvos)
dc.contributor.authorRacskó Márk (2024-) (xxx)
dc.contributor.authorKelemen Balázs (1992-) (biológus)
dc.contributor.authorKovalecz Gabriella (1973-) (fog és szájbetegségek szakorvosa, gyermekfogászat szakorvosa, konzerváló fogászat és fogpótlástan szakorvosa, endodontia szakorvosa)
dc.contributor.authorD. Tóth Etelka (1975-) (fogszakorvos)
dc.contributor.authorHegedűs Csaba (1953-) (fogszakorvos)
dc.contributor.authorBágyi Kinga (1971-) (fogszakorvos)
dc.contributor.authorMarincsák Rita (1979-) (fogszakorvos)
dc.contributor.authorTóth István Balázs (1978-) (élettanász)
dc.contributor.submitterdepÉlettani Intézet -- 10
dc.contributor.submitterdepKonzerváló Fogászati nem önálló Tanszék -- 206
dc.contributor.submitterdepGyermekfogászati és Prevenciós nem önálló Tanszék -- 4388
dc.contributor.submitterdepDentoalveoláris Sebészeti nem önálló Tanszék -- 4387
dc.contributor.submitterdepBioanyagtani és Fogpótlástani Nem Önálló Tanszék -- 203
dc.contributor.submitterdepÁOK
dc.contributor.submitterdepFOK
dc.contributor.submitterdepDebreceni Egyetem
dc.date.accessioned2024-07-15T09:25:13Z
dc.date.available2024-07-15T09:25:13Z
dc.date.oa2024-09-19
dc.date.updated2024-07-15T09:25:13Z
dc.description.abstractBackground and Purpose: Pulpitis is associated with tooth hypersensitivity and results in pulpal damage. Thermosensitive transient receptor potential (TRP) ion channels expressed in the dental pulp may be key transducers of inflammation and nociception. We aimed at investigating the expression and role of thermo-TRPs in primary human dental pulp cells (hDPCs) in normal and inflammatory conditions. Experimental Approach: Inflammatory conditions were induced in hDPC cultures by applying polyinosinic:polycytidylic acid (poly(I:C)). Gene expression and pro-inflammatory cytokine release were measured by RT-qPCR and ELISA. Functions of TRPA1 channels were investigated by monitoring changes in intracellular Ca2+ concentration. Mitochondrial superoxide production was measured using a fluorescent substrate. Cellular viability was assessed by measuring the activity of mitochondrial dehydrogenases and cytoplasmic esterases. TRPA1 activity was modified by agonists, antagonists, and gene silencing. Key Results: Transcripts of TRPV1, TRPV2, TRPV4, TRPC5, and TRPA1 were highly expressed in control hDPCs, whereas TRPV3, TRPM2, and TRPM3 expressions were much lower, and TRPM8 was not detected. Poly(I:C) markedly up-regulated TRPA1 but not other thermo-TRPs. TRPA1 agonist-induced Ca2+ signals were highly potentiated in inflammatory conditions. Poly(I:C)-treated cells displayed increased Ca2+ responses to H2O2, which was abolished by TRPA1 antagonists. Inflammatory conditions induced oxidative stress, stimulated mitochondrial superoxide production, resulted in mitochondrial damage, and decreased cellular viability of hDPCs. This inflammatory cellular damage was partly prevented by the co-application of TRPA1 antagonist or TRPA1 silencing. Conclusion and Implications: Pharmacological blockade of TRPA1 channels may be a promising therapeutic approach to alleviate pulpitis and inflammation-associated pulpal damage. © 2024 The Authors. British Journal of Pharmacology published by John Wiley & Sons Ltd on behalf of British Pharmacological Society.
dc.description.correctorkzs
dc.identifier.citationBritish Journal Of Pharmacology. -2024 (2024), p. 1-17. -Br. J. Pharmacol. -0007-1188
dc.identifier.doi10.1111/bph.16386
dc.identifier.issn0007-1188
dc.identifier.opachttps://ebib.lib.unideb.hu/ebib/CorvinaWeb?action=cclfind&resultview=long&ccltext=idno+BIBFORM122715
dc.identifier.urihttps://hdl.handle.net/2437/375582
dc.identifier.urlhttps://bpspubs.onlinelibrary.wiley.com/doi/10.1111/bph.16386
dc.languageeng
dc.rights.accessopen access article
dc.rights.ownerszerző
dc.subject.otheridegen nyelvű folyóiratközlemény külföldi lapban
dc.subject.otherdental pulp
dc.subject.otherendodontics
dc.subject.otherimmunopharmacology
dc.subject.otherinflammation
dc.subject.otherreactive oxygen species
dc.subject.othertransient receptor potential channels
dc.subject.otherTRPA1
dc.title[S] TRPA1 up‐regulation mediates oxidative stress in a pulpitis model in vitro
Fájlok
Eredeti köteg (ORIGINAL bundle)
Megjelenítve 1 - 1 (Összesen 1)
Nincs kép
Név:
FILE_UP_0_British J Pharmacology - 2024 - Kunka - TRPA1 up‐regulation mediates oxidative stress in a pulpitis model in vitro.pdf
Méret:
3.38 MB
Formátum:
Adobe Portable Document Format
Leírás:
kiadói változat
Letöltés
Gyűjtemények
Publikációs Adatbázis