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001-es BibID:BIBFORM120201
035-os BibID:(Scopus)85190549139 (WoS)001204438100001
Első szerző:Cozzolino, Marco (biológus)
Cím:Intracellular acidity impedes KCa3.1 activation by Riluzole and SKA-31 / Cozzolino Marco, Panyi Gyorgy
Dátum:2024
ISSN:1663-9812
Megjegyzések:Based on our data we conclude that KCa3.1 currents are not sensitive the either the intracellular or the extracellular pH in the physiological and pathophysiological range. However, intracellular acidosis in T cells residing in the tumor microenvironment could hinder the potentiating effect of KCa3.1 positive modulators administered to boost their activity. Further research is warranted both to clarify the molecular interactions between the modulators and KCa3.1 at different intracellular pH conditions and to define whether this loss of potency can be observed in cancer models as well.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
ion channels
KCa3.1
Riluzole
SKA-31
acidity
cancer
Megjelenés:Frontiers in Pharmacology. - 15 (2024), p. 1-23. -
További szerzők:Panyi György (1966-) (biofizikus)
Pályázati támogatás:K119417
OTKA
813834-pHioniC-H2020-MSCA-ITN-2018
Egyéb
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2.

001-es BibID:BIBFORM110227
035-os BibID:(cikkazonosító)6216 (Scopus)85152336402 (WoS)000969756600001
Első szerző:Cozzolino, Marco (biológus)
Cím:The Voltage-Gated Hv1 H⁺ Channel Is Expressed in Tumor-Infiltrating Myeloid-Derived Suppressor Cells / Cozzolino Marco, Gyöngyösi Adrienn, Korpos Eva, Gogolak Peter, Naseem Muhammad Umair, Kállai Judit, Lanyi Arpad, Panyi Gyorgy
Dátum:2023
ISSN:1422-0067
Megjegyzések:Myeloid-derived suppressor cells (MDSCs) are key determinants of the immunosuppressive microenvironment in tumors. As ion channels play key roles in the physiology/pathophysiology of immune cells, we aimed at studying the ion channel repertoire in tumor-derived polymorphonuclear (PMN-MDSC) and monocytic (Mo-MDSC) MDSCs. Subcutaneous tumors in mice were induced by the Lewis lung carcinoma cell line (LLC). The presence of PMN-MDSC (CD11b+/Ly6G+) and Mo-MDSCs (CD11b+/Ly6C+) in the tumor tissue was confirmed using immunofluorescence microscopy and cells were identified as CD11b+/Ly6G+ PMN-MDSCs and CD11b+/Ly6C+/F4/80?/MHCII? Mo-MDSCs using flow cytometry and sorting. The majority of the myeloid cells infiltrating the LLC tumors were PMN-MDSC (~60%) as compared to ~10% being Mo-MDSCs. We showed that PMN- and Mo-MDSCs express the Hv1 H+ channel both at the mRNA and at the protein level and that the biophysical and pharmacological properties of the whole-cell currents recapitulate the hallmarks of Hv1 currents: ~40 mV shift in the activation threshold of the current per unit change in the extracellular pH, high H+ selectivity, and sensitivity to the Hv1 inhibitor ClGBI. As MDSCs exert immunosuppression mainly by producing reactive oxygen species which is coupled to Hv1-mediated H+ currents, Hv1 might be an attractive target for inhibition of MDSCs in tumors.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Myeloid-derived suppressor cell
Hv1 proton channel
tumor microenvironment
Megjelenés:International Journal Of Molecular Sciences. - 24 : 7 (2023), p. 1-24. -
További szerzők:Gyöngyösi Adrienn (1982-) (biológus) Korpos Éva (1974-) Gogolák Péter (1968-) (biológus, immunológus) Naseem, Muhammad Umair (1993-) (biofizikus, molekuláris biológus) Kállai Judit (1983-) (molekuláris biológus) Lányi Árpád (1962-) (biológus, immunológus) Panyi György (1966-) (biofizikus)
Pályázati támogatás:K119417
OTKA
K131708
OTKA
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Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM091510
035-os BibID:(cikkazonosító)586599 (scopus)85102899354 (wos)000615362700001
Első szerző:Hofschröer, Verena
Cím:Ion Channels Orchestrate Pancreatic Ductal Adenocarcinoma Progression and Therapy / Hofschröer Verena, Najder Karolina, Rugi Micol, Bouazzi Rayhana, Cozzolino Marco, Arcangeli Annarosa, Panyi Gyorgy, Schwab Albrecht
Dátum:2021
ISSN:1663-9812
Megjegyzések:Pancreatic ductal adenocarcinoma is a devastating disease with a dismal prognosis. Therapeutic interventions are largely ineffective. A better understanding of the pathophysiology is required. Ion channels contribute substantially to the "hallmarks of cancer." Their expression is dysregulated in cancer, and they are "misused" to drive cancer progression, but the underlying mechanisms are unclear. Ion channels are located in the cell membrane at the interface between the intracellular and extracellular space. They sense and modify the tumor microenvironment which in itself is a driver of PDAC aggressiveness. Ion channels detect, for example, locally altered proton and electrolyte concentrations or mechanical stimuli and transduce signals triggered by these microenvironmental cues through association with intracellular signaling cascades. While these concepts have been firmly established for other cancers, evidence has emerged only recently that ion channels are drivers of PDAC aggressiveness. Particularly, they appear to contribute to two of the characteristic PDAC features: the massive fibrosis of the tumor stroma (desmoplasia) and the efficient immune evasion. Our critical review of the literature clearly shows that there is still a remarkable lack of knowledge with respect to the contribution of ion channels to these two typical PDAC properties. Yet, we can draw parallels from ion channel research in other fibrotic and inflammatory diseases. Evidence is accumulating that pancreatic stellate cells express the same "profibrotic" ion channels. Similarly, it is at least in part known which major ion channels are expressed in those innate and adaptive immune cells that populate the PDAC microenvironment. We explore potential therapeutic avenues derived thereof. Since drugs targeting PDAC-relevant ion channels are already in clinical use, we propose to repurpose those in PDAC. The quest for ion channel targets is both motivated and complicated by the fact that some of the relevant channels, for example, KCa3.1, are functionally expressed in the cancer, stroma, and immune cells. Only in vivo studies will reveal which arm of the balance we should put our weights on when developing channeltargeting PDAC therapies. The time is up to explore the efficacy of ion channel targeting in (transgenic) murine PDAC models before launching clinical trials with repurposed drugs
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
pancreatic ductal adenocarcinoma
ion channels
therapy
immune cells
fibrosis
Megjelenés:Frontiers in Pharmacology. - 11 (2021), p. 1-28. -
További szerzők:Najder, Karolina Rugi, Micol Bouazzi, Rayhana Cozzolino, Marco (1991-) (biológus) Arcangeli, Annarosa Panyi György (1966-) (biofizikus) Schwab, Albrecht
Pályázati támogatás:Marie Skodowska-Curie Innovative Training Network (ITN) - 813834 - pHioniC - H2020-MSCA-ITN-2018
Egyéb
K119417
OTKA
EFOP-3.6.2-16-2017-00006
EFOP
GINOP-2.3.2-15-2016-00015
GINOP
AIRC, Grant N? IG 15627 and IG 21510 to AA, PRIN Italian Ministry of University and Research (MIUR)
Egyéb
LIONESS 20174TB8KW
Egyéb
DFG; SCHW 407/17-1 & SCHW 407/22-1; GRK 2515/1, Chembion
Egyéb
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4.

001-es BibID:BIBFORM100558
035-os BibID:(WoS)000758208100001 (Scopus)85124886681
Első szerző:Somodi Laura (klinikai laboratóriumi kutató)
Cím:Activation mechanism dependent surface exposure of cellular factor XIII on activated platelets and platelet microparticles / Somodi Laura, Beke Debreceni Ildikó, Kis Gréta, Cozzolino Marco, Kappelmayer János, Antal Miklós, Panyi György, Bárdos Helga, Mutch Nicola J., Muszbek, László
Dátum:2022
ISSN:1538-7933 1538-7836
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Journal Of Thrombosis And Haemostasis. - 20 : 5 (2022), p. 1223-1235. -
További szerzők:Bekéné Debreceni Ildikó (1970-) (biológus) Kis Gréta (1979-) (molekuláris biológus) Cozzolino, Marco (1991-) (biológus) Kappelmayer János (1960-) (laboratóriumi szakorvos) Antal Miklós (1951-) (orvos, anatómus) Panyi György (1966-) (biofizikus) Bárdos Helga (1969-) (megelőző orvostan és népegészségtan szakorvos) Mutch, Nicola J. Muszbek László (1942-) (haematológus, kutató orvos)
Pályázati támogatás:GINOP-2.3.2-15-2016-00050
GINOP
NKFIH-K129287
Egyéb
11014 project
MTA
British Heart Foundation-PG/15/82/31721/BHF_/
Egyéb
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Intézményi repozitóriumban (DEA) tárolt változat
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