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001-es BibID:	BIBFORM118970
Első szerző:	Kunka Árpád (arc-, állcsont- és szájsebész)
Cím:	TRPA1 upregulation mediates oxidative stress in a pulpitis model in vitro / Árpád Kunka, Erika Lisztes, Judit Bohács, Márk Racskó, Balázs Kelemen, Gabriella Kovalecz, Etelka D. Tóth, Csaba Hegedűs, Kinga Bágyi, Rita Marincsák, Balázs István Tóth
Dátum:	2024
ISSN:	0007-1188
Megjegyzések:	BACKGROUND 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 proinflammatory cytokine-release were measured by RT-qPCR and ELISA. Function of TRPA1 was investigated by monitoring changes in intracellular Ca2+ concentration. Mitochondrial superoxide production was measured using a fluorescent substrate and cellular viability was assessed by measuring the activity of mitochondrial dehydrogenases and cytoplasmic esterases. TRPA1 activity was manipulated by agonists, antagonists, and gene silencing. KEY RESULTS The 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 upregulated 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 antagonism. Inflammatory conditions induced oxidative stress, stimulated mitochondrial superoxide production, resulted in mitochondrial damage, and decreased cellular viability of hDPCs. This inflammatory cellular damage was partially prevented by the co-application of TRPA1 antagonist or TRPA1 silencing. CONCLUSION AND IMPLICATIONS The pharmacological blockade of TRPA1 may be a promising therapeutic approach to alleviate pulpitis and inflammation-associated pulpal damage.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Immunopharmacology Inflammation Transient Receptor Potential Channels TRPA1 Dental Pulp Reactive Oxygen Species Endodontics
Megjelenés:	British Journal of Pharmacology. - "Accepted by Publisher" (2024), p. 126-131. -
További szerzők:	Lisztes Erika (1986-) (élettanász) Bohács Judit (1993-) (fogorvos) Racskó Márk (1991-) (molekuláris biológus) Kelemen Balázs (1992-) (biológus) Kovalecz Gabriella (1973-) (fogszakorvos) D. Tóth Etelka (1975-) (fogszakorvos) Hegedűs Csaba (1953-) (fogszakorvos) Bágyi Kinga (1971-) (fogszakorvos) Marincsák Rita (1979-) (fogszakorvos) Tóth István Balázs (1978-) (élettanász)
Pályázati támogatás:	134725 OTKA 134791 OTKA EFOP-3.6.1-16-2016-00022 EFOP GINOP-2.3.2-15-2016-00050 GINOP ÚNKP-22-3-I-DE-324 Egyéb ÚNKP-21-5-DE-491 Egyéb János Bolyai Research Scholarship of the Hungarian Academy of Sciences Egyéb
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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