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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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2.

001-es BibID:BIBFORM037346
Első szerző:Szentandrássy Norbert (élettanász)
Cím:Role of action potential configuration and the contribution of Ca2+ and K+ currents to isoprenaline-induced changes in canine ventricular cells / N. Szentandrássy, V. Farkas, L. Bárándi, B. Hegyi, F. Ruzsnavszky, B. Horváth, T. Bányász, J. Magyar, I. Márton, P. P. Nánási
Dátum:2012
ISSN:0007-1188
Megjegyzések:BACKGROUND AND PURPOSE: Although isoprenaline (ISO) is known to activate several ion currents in mammalian myocardium, little is known about the role of action potential morphology in the ISO-induced changes in ion currents. Therefore, the effects of ISO on action potential configuration, L-type Ca2+ current (ICa), slow delayed rectifier K+ current (IKs) and fast delayed rectifier K+ current (IKr)were studied and compared in a frequency-dependent manner using canine isolated ventricular myocytes from varioustransmural locations.EXPERIMENTAL APPROACHAction potentials were recorded with conventional sharp microelectrodes; ion currents were measured using conventional and action potential voltage clamp techniques.KEY RESULTSIn myocytes displaying a spike-and-dome action potential configuration (epicardial and midmyocardial cells), ISO caused reversible shortening of action potentials accompanied by elevation of the plateau. ISO-induced action potential shortening was absent in endocardial cells and in myocytes pretreated with 4-aminopyridine. Application of the IKr blocker E-4031 failed to modify the ISO effect, while action potentials were lengthened by ISO in the presence of the IKs blocker HMR-1556. Bothaction potential shortening and elevation of the plateau were prevented by pretreatment with the ICa blocker nisoldipine.Action potential voltage clamp experiments revealed a prominent slowly inactivating ICa followed by a rise in IKs, both currents increased with increasing the cycle length.CONCLUSIONS AND IMPLICATIONSThe effect of ISO in canine ventricular cells depends critically on action potential configuration, and the ISO-induced activation of IKs ? but not IKr ? may be responsible for the observed shortening of action potentials
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
heart
action potential
calcium current
potassium current
Megjelenés:British Journal of Pharmacology. - 167 : 3 (2012), p. 599-611. -
További szerzők:Farkas Viktória Bárándi László (1984-) (élettanász) Hegyi Bence (1987-) (élettanász) Ruzsnavszky Ferenc (1984-) (élettanász) Horváth Balázs (1981-) (élettanász) Bányász Tamás (1960-) (élettanász) Magyar János (1961-) (élettanász) Márton Ildikó (1954-) (fogszakorvos) Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
A feszültségfüggő K-csatornák szerepe excitábilis sejtekben
Internet cím:DOI
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