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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
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM111194
035-os BibID:	(cikkazonosító)656 (WoS)000996659300001 (Scopus)85160676201
Első szerző:	Szántó Gábor Tibor (vegyész)
Cím:	5-Chloro-2-Guanidinobenzimidazole (ClGBI) Is a Non-Selective Inhibitor of the Human HV1 Channel / Szanto Tibor G., Feher Adam, Korpos Eva, Gyöngyösi Adrienn, Kállai Judit, Mészáros Beáta, Ovari Krisztian, Lányi Árpád, Panyi Gyorgy, Varga Zoltan
Dátum:	2023
ISSN:	1424-8247
Megjegyzések:	5-chloro-2-guanidinobenzimidazole (ClGBI), a small-molecule guanidine derivative, is a known effective inhibitor of the voltage-gated proton (H+) channel (H(V)1, K-d approximate to 26 mu M) and is widely used both in ion channel research and functional biological assays. However, a comprehensive study of its ion channel selectivity determined by electrophysiological methods has not been published yet. The lack of selectivity may lead to incorrect conclusions regarding the role of hHv1 in physiological or pathophysiological responses in vitro and in vivo. We have found that ClGBI inhibits the proliferation of lymphocytes, which absolutely requires the functioning of the K(V)1.3 channel. We, therefore, tested ClGBI directly on hK(V)1.3 using a whole-cell patch clamp and found an inhibitory effect similar in magnitude to that seen on hH(V)1 (K-d approximate to 72 mu M). We then further investigated ClGBI selectivity on the hK(V)1.1, hK(V)1.4-IR, hK(V)1.5, hK(V)10.1, hK(V)11.1, hK(Ca)3.1, hNa(V)1.4, and hNa(V)1.5 channels. Our results show that, besides H(V)1 and K(V)1.3, all other off-target channels were inhibited by ClGBI, with K-d values ranging from 12 to 894 mu M. Based on our comprehensive data, ClGBI has to be considered a non-selective hH(V)1 inhibitor; thus, experiments aiming at elucidating the significance of these channels in physiological responses have to be carefully evaluated.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk ClGBI proton channel voltage-gated ion channels blocking kinetics selectivity screening
Megjelenés:	Pharmaceuticals. - 16 : 5 (2023), p. 1-15. -
További szerzők:	Fehér Ádám (1996-) (orvos, biofizikus) Korpos Éva (1974-) Gyöngyösi Adrienn (1982-) (biológus) Kállai Judit (1983-) (molekuláris biológus) Mészáros Beáta (1985-) (molekuláris biológus, mikrobiológus) Óvári Krisztián Lányi Árpád (1962-) (biológus, immunológus) Panyi György (1966-) (biofizikus) Varga Zoltán (1969-) (biofizikus, szakfordító)
Pályázati támogatás:	K132906 OTKA 2019-2.1.11-TÉT-2019-00059, TÉT, NKFIH Egyéb K131708 OTKA K143071 OTKA ÚNKP-22-3-II-DE-38 New National Excellence Program of the Ministry for Culture and Innovation Egyéb
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