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1.

001-es BibID:BIBFORM070903
Első szerző:Ambrus Lídia (élettanász)
Cím:Human podocytes express functional thermosensitive transient receptor potential vanilloid (TRPV) channels / Lídia Ambrus, Balázs Kelemen, Tamás Szabó, Tamás Bíró, Balázs István Tóth
Dátum:2017
ISSN:0007-1188
Megjegyzések:BACKGROUND AND PURPOSEHeat sensitive transient receptor potential vanilloid (TRPV) channels are expressed in various epithelial tissues regulating, among else, barrier functions. Their expression is well established in the distal nephron; however, we have no data about their presence in podocytes. Since podocytes are indispensable in the formation of the glomerular filtration barrier, we investigated the presence and function of Ca2+-permeable TRPV1-4 channels in human podocyte cultures.EXPERIMENTAL APPROACHThe expression of TRPV1-4 was investigated at protein (immunocytochemistry, western blot) and mRNA (Q-PCR) level in a conditionally immortalized human podocyte cell line. The channel functionality was assessed by measuring intracellular Ca2+ concentration using fluo-4 Ca2+-indicator dye and patch clamp electrophysiology upon applying various activators and inhibitors.KEY RESULTSThermosensitive TRP channels were expressed in podocytes. The TRPV1 specific agonists capsaicin and resiniferatoxin did not induce any alteration in the intracellular Ca2+ concentration. Cannabidiol, an activator of TRPV2 and TRPV4 induced moderate Ca2+-influxes which were inhibited by both tranilast and HC067047, blockers of TRPV2 and TRPV4, respectively. The TRPV4-specific agonists GSK1016790A and 4?-Phorbol 12,13-didecanoate resulted robust Ca2+-signals which were abolished in the presence of HC067047. Non-specific agonists of TRPV3 induced marked Ca2+ transients. However, TRPV3 blockers, ruthenium red and isopentenyl diphosphate only partially inhibited the responses and TRPV3 silencing was ineffective suggesting remarkable off-target effects of the compounds.CONCLUSION AND IMPLICATIONSOur results indicate the functional presence of TRPV4 and other thermosensitive TRPV channels in human podocytes and raise the possibility of their involvement in the regulation of glomerular filtration barrier.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:British journal of pharmacology. - 174 : 23 (2017), p. 4493-4507. -
További szerzők:Kelemen Balázs (1992-) (biológus) Szabó Tamás (1968-) (gyermekgyógyász) Bíró Tamás (1968-) (élettanász) Tóth István Balázs (1978-) (élettanász)
Pályázati támogatás:76065
OTKA
NKFI K_16 120187
Egyéb
NKFI K_16 120552
Egyéb
TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
LP003-2011/2015
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM089428
035-os BibID:(cikkazonosító)114310 (Scopus)85097002422 (WOS)000604265300002 (PubMed)33130130
Első szerző:Kelemen Balázs (biológus)
Cím:The TRPM3 ion channel mediates nociception but not itch evoked by endogenous pruritogenic mediators / Balázs Kelemen, Silvia Pinto, Nawoo Kim, Erika Lisztes, Martin Hanyicska, Anita Vladár, Attila Oláh, Zsófia Pénzes, Brian Shu, Joris Vriens, Tamás Bíró, Tibor Rohács, Thomas Voets, Balázs István Tóth
Dátum:2021
ISSN:0006-2952
Megjegyzések:During the molecular transduction of itch, the stimulation of pruriceptors on sensory fibers leads to the activation or sensitization of ion channels, which results in a consequent depolarization of the neurons. These ion channels mostly belong to the transient receptor potential (TRP) channels, which are involved in nociception and thermosensation. In particular, TRPV1 and TRPA1 were described in the transduction of both thermal nociception as well as histaminergic and non-histaminergic itch. The thermosensitive TRPM3 plays an indispensable role in heat nociception together with TRPV1 and TRPA1. However, the role of TRPM3 in the development of pruritus has not been studied yet. Therefore, in this study we aimed at investigating the potential role of TRPM3 in the transduction of pruritus and pain by investigating itch- and nociception-related behavior of Trpm3+/+ and Trpm3?/? mice, and by studying the activation of somatosensory neurons isolated from trigeminal ganglia upon application of algogenic and pruritogenic substances. Activators of TRPM3 evoked only nocifensive responses, but not itch in Trpm3+/+ animals, and these nocifensive responses were abolished in the Trpm3?/? strain. Histamine and endogenous non-histaminergic pruritogens induced itch in both Trpm3+/+ and Trpm3?/? mice to a similar extent. Genetic deletion or pharmacological blockade diminished TRPM3 mediated Ca2+ responses of sensory neurons, but did not affect responses evoked by pruritogenic substances. Our results demonstrate that, in contrast to other thermosensitive TRP channels, TRPM3 selectively mediates nociception, but not itch sensation, and suggest that TRPM3 is a promising candidate to selectively target pain sensation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Nociception
Itch
TRP channels
TRPM3
Cheek model
Endogenous pruritogens
Megjelenés:Biochemical Pharmacology. - 183 (2021), p. 114310. -
További szerzők:Pinto, Silvia Kim, Nawoo Lisztes Erika (1986-) (élettanász) Hanyicska Martin (1992-) (biotechnológus) Vladár Anita Oláh Attila (1984-) (élettanász) Pénzes Zsófia (1992-) (klinikai laboratóriumi kutató) Shu, Brian Vriens, Joris Bíró Tamás (1968-) (élettanász) Rohács Tibor Voets, Thomas Tóth István Balázs (1978-) (élettanász)
Pályázati támogatás:K_120187
OTKA
PD_121360
OTKA
PD-134791
OTKA
FK_125055
OTKA
GINOP-2.3.2-15-2016-00015
GINOP
EFOP-3.6.3- VEKOP-16-2017-00009
EFOP
EFOP-3.6.1-16-2016-00022
EFOP
ÚNKP-20-5-DE-422
ÚNKP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM083138
035-os BibID:(Scopus)85079239909 (WOS)000527342900032 (cikkazonosító)113826 (PubMed)31987857
Első szerző:Kelemen Balázs (biológus)
Cím:Volatile anaesthetics inhibit the thermosensitive nociceptor ion channel transient receptor potential melastatin 3 (TRPM3) / Balázs Kelemen, Erika Lisztes, Anita Vladár, Martin Hanyicska, János Almássy, Attila Oláh, Attila Gábor Szöllősi, Zsófia Pénzes, János Posta, Thomas Voets, Tamás Bíró, Balázs István Tóth
Dátum:2020
ISSN:0006-2952
Megjegyzések:Background Volatile anaesthetics (VAs) are the most widely used compounds to induce reversible loss of consciousness and maintain general anaesthesia during surgical interventions. Although the mechanism of their action is not yet fully understood, it is generally believed, that VAs depress central nervous system functions mainly through modulation of ion channels in the neuronal membrane, including 2-pore-domain K+ channels, GABA and NMDA receptors. Recent research also reported their action on nociceptive and thermosensitive TRP channels expressed in the peripheral nervous system, including TRPV1, TRPA1, and TRPM8. Here, we investigated the effect of VAs on TRPM3, a less characterized member of the thermosensitive TRP channels playing a central role in noxious heat sensation. Methods We investigated the effect of VAs on the activity of recombinant and native TRPM3, by monitoring changes in the intracellular Ca2+ concentration and measuring TRPM3-mediated transmembrane currents. Results All the investigated VAs (chloroform, halothane, isoflurane, sevoflurane) inhibited both the agonist-induced (pregnenolone sulfate, CIM0216) and heat-activated Ca2+ signals and transmembrane currents in a concentration dependent way in HEK293T cells overexpressing recombinant TRPM3. Among the tested VAs, halothane was the most potent blocker (IC50=0.52?0.05 mM). We also investigated the effect of VAs on native TRPM3 channels expressed in sensory neurons of the dorsal root ganglia. While VAs activated certain sensory neurons independently of TRPM3, they strongly and reversibly inhibited the agonist-induced TRPM3 activity. Conclusions These data provide a better insight into the molecular mechanism beyond the analgesic effect of VAs and propose novel strategies to attenuate TRPM3 dependent nociception.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Volatile anaesthetics
TRP ion channels
TRPM3
Nociception
Thermosensation
Megjelenés:Biochemical Pharmacology. - 174 (2020), p. 113826. -
További szerzők:Lisztes Erika (1986-) (élettanász) Vladár Anita Hanyicska Martin (1992-) (biotechnológus) Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító) Oláh Attila (1984-) (élettanász) Szöllősi Attila Gábor (1982-) (élettanász) Pénzes Zsófia (1992-) (klinikai laboratóriumi kutató) Posta János (1964-) (vegyész, toxikológus) Voets, Thomas Bíró Tamás (1968-) (élettanász) Tóth István Balázs (1978-) (élettanász)
Pályázati támogatás:GINOP-2.3.2-15-2016-00050
GINOP
ÚNKP-19-4-DE-287
Egyéb
ÚNKP-19-4-DE-142
Egyéb
ÚNKP-19-3-I-DE-140
Egyéb
ÚNKP-19-4-DE-285
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM075069
035-os BibID:(WOS)000439136200026 (Scopus)85047087852
Első szerző:Kemény Ágnes
Cím:TRPA1 Acts in a Protective Manner in Imiquimod-Induced Psoriasiform Dermatitis in Mice / Ágnes Kemény, Xenia Kodji, Szabina Horváth, Rita Komlódi, Éva Szőke, Zoltán Sándor, Anikó Perkecz, Csaba Gyömörei, György Sétáló, Balázs Kelemen, Tamás Bíró, Balázs István Tóth, Susan D. Brain, Erika Pintér, Rolland Gyulai
Dátum:2018
ISSN:0022-202X 1523-1747
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Journal of Investigative Dermatology. - 138 : 8 (2018), p. 1774-1784. -
További szerzők:Kodji, Xenia Horváth Szabina Komlódi Rita Szőke Éva Sándor Zoltán (Pécs) Perkecz Anikó Gyömörei Csaba Sétáló György Kelemen Balázs (1992-) (biológus) Bíró Tamás (1968-) (élettanász) Tóth István Balázs (1978-) (élettanász) Brain, Susan D. Pintér Erika Gyulai Rolland
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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5.

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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6.

001-es BibID:BIBFORM119089
Első szerző:Tóth István Balázs (élettanász)
Cím:Direct modulation of TRPM8 ion channels by rapamycin and analog macrolide immunosuppressants / Balázs István Tóth, Bahar Bazeli, Annelies Janssens, Erika Lisztes, Márk Racskó, Balázs Kelemen, Mihály Herczeg, Tamás Milán Nagy, Katalin E. Kövér, Argha Mitra, Attila Borics, Tamás Bíró, Thomas Voets
Dátum:2024
ISSN:2050-084X
Megjegyzések:Rapamycin (sirolimus), a macrolide compound isolated from the bacterium Streptomyces hygroscopicus, is widely used as oral medication for the prevention of transplant rejection and the treatment of lymphangioleiomyomatosis. It is also incorporated in coronary stent coatings to prevent restenosis and in topical preparations for the treatment of skin disorders. Rapamycin's in vivo activities are generally ascribed to its binding to the protein FKBP12, leading to potent inhibition of the mechanistic target of rapamycin kinase (mTOR) by the FKBP12-rapamycin complex. The specific rapamycin-induced interaction between domains from mTOR and FKBP12 is also frequently employed in cell biological research, for rapid chemically-induced protein dimerization strategies. Here we show that rapamycin activates TRPM8, a cation channel expressed in sensory nerve endings that serves as the primary cold sensor in mammals. Using a combination of electrophysiology, Saturation Transfer Triple-Difference (STTD) NMR spectroscopy and molecular docking-based targeted mutagenesis, we demonstrate that rapamycin directly binds to TRPM8. We identify a rapamycin-binding site in the groove between voltage sensor-like domain and the pore domain, distinct from the interaction sites of cooling agents and known TRPM8 agonists menthol and icilin. Related macrolide immunosuppressants act as partial TRPM8 agonists, competing with rapamycin for the same binding site. These findings identify a novel molecular target for rapamycin and provide new insights into the mechanisms of TRPM8 activation, which may assist in the development of therapies targeting this ion channel. Moreover, our findings also indicate that caution is needed when using molecular approaches based on rapamycin-induced dimerization to study ion channel regulation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
TRPM8
Rapamycin
Electrophysiology
NMR spectroscopy
Neuroscience
Megjelenés:eLife. - "Accepted by Publisher" (2024). -
További szerzők:Bazeli, Bahar Janssens, Annelies Lisztes Erika (1986-) (élettanász) Racskó Márk (1991-) (molekuláris biológus) Kelemen Balázs (1992-) (biológus) Herczeg Mihály (1979-) (vegyész, biológia-kémia tanár) Nagy Tamás Milán (1993-) (vegyész, nmr) Kövér Katalin, E. (1956-2023) (vegyész) Mitra, Argha Borics Attila Bíró Tamás (1968-) (élettanász) Voets, Thomas
Pályázati támogatás:134725
OTKA
134791
OTKA
128368
OTKA
137924
OTKA
GINOP-2.3.2-15-2016-00050
GINOP
GINOP-2.3.3-15-2016-00004
GINOP
GINOP-2.2.1-15-2017-00044
GINOP
János Bolyai Research Scholarship
Egyéb
ÚNKP-22-3-I-DE-324
Egyéb
ÚNKP-23-3-II-DE-430
Egyéb
UNKP-22-4-I-DE-87
Egyéb
ÚNKP-21-5-DE-491
Egyéb
FWO; G0B9520N
Egyéb
FWO; G0B7620N
Egyéb
esearch Council of KU Leuven (C2-TRP)
Egyéb
Queen Elisabeth Medical Foundation for Neurosciences
Egyéb
EU's Horizon 2020 research and innovation program under grant agreement No. 739593
Egyéb
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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