TY - JOUR AU - Isotta, Sturniolo AU - Csongor, Váróczy AU - Ákos, Máté Bede AU - Hegedűs, Csaba AU - Demény, Máté Ágoston AU - Virág, László TI - Quantifying antibody-dependent cellular cytotoxicity in a tumor spheroid model : application for drug discovery JF - JOVE-JOURNAL OF VISUALIZED EXPERIMENTS J2 - JOVE-J VIS EXP PY - 2024 SN - 1940-087X UR - https://m2.mtmt.hu/api/publication/34820104 ID - 34820104 LA - English DB - MTMT ER - TY - JOUR AU - Sturniolo, I AU - Váróczy, Cs AU - Regdon, Zsolt AU - Mázló, A AU - Muzsai, Sz AU - Bácsi, A AU - Intili, G AU - Hegedűs, Csaba AU - Boothby, MR AU - Holechek, J AU - Ferraris, D AU - Schüler, H AU - Virág, László TI - PARP14 contributes to the development of the tumor-associated macrophage phenotype JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 25 PY - 2024 IS - 7 SP - 1 EP - 21 PG - 21 SN - 1661-6596 DO - 10.3390/ijms25073601 UR - https://m2.mtmt.hu/api/publication/34754751 ID - 34754751 LA - English DB - MTMT ER - TY - JOUR AU - Virág, László AU - Hegedűs, Csaba AU - Kovács, Katalin AU - Polgár, Zsuzsanna AU - Kókai, Endre AU - Sturniolo, Isotta AU - Demény, Máté Ágoston AU - Virág, Bernadett AU - Szabó, Éva TI - Automated high-throughput cell culture scratch assay identifies wound healing promoting and inhibiting compounds from a small compound library of redox active molecules JF - FREE RADICAL BIOLOGY AND MEDICINE J2 - FREE RADICAL BIO MED VL - 208 PY - 2023 SP - S144 EP - S144 PG - 1 SN - 0891-5849 DO - 10.1016/j.freeradbiomed.2023.10.328 UR - https://m2.mtmt.hu/api/publication/34729573 ID - 34729573 LA - English DB - MTMT ER - TY - JOUR AU - Guti, Eliza AU - Bede, Ákos Máté AU - Váróczy, Csongor AU - Hegedűs, Csaba AU - Demény, Máté Ágoston AU - Virág, László TI - High-Content Screening Assay for the Identification of Antibody-Dependent Cellular Cytotoxicity Modifying Compounds JF - JOVE-JOURNAL OF VISUALIZED EXPERIMENTS J2 - JOVE-J VIS EXP PY - 2023 IS - 198 SP - 1 EP - 12 PG - 12 SN - 1940-087X DO - 10.3791/64485 UR - https://m2.mtmt.hu/api/publication/34108111 ID - 34108111 LA - English DB - MTMT ER - TY - JOUR AU - Skopál, Adrienn AU - Ujlaki, Gyula AU - Gerencsér, Attila Tibor AU - Bankó, Csaba AU - Bacsó, Zsolt AU - Ciruela, Francisco AU - Virág, László AU - Haskó, György AU - Kókai, Endre TI - Adenosine A2A Receptor Activation Regulates Niemann–Pick C1 Expression and Localization in Macrophages JF - CURRENT ISSUES IN MOLECULAR BIOLOGY J2 - CURR ISSUES MOL BIOL VL - 45 PY - 2023 IS - 6 SP - 4948 EP - 4969 PG - 22 SN - 1467-3037 DO - 10.3390/cimb45060315 UR - https://m2.mtmt.hu/api/publication/34020857 ID - 34020857 N1 - Funding Agency and Grant Number: National Research Development and Innovation Office [OTKA MB08A 84685, GINOP-2.3.2-15-2016-00020 TUMORDNS, R01GM066189]; National Research, Development and Innovation Office [K147482, GINOP-2.3.2-15-2016-00048-STAYALIVE]; National Institutes of Health [R01DK113790, R01HL158519]; [OTKA K132193] Funding text: EK received funding from National Research Development and Innovation Office OTKA MB08A 84685; LV received funding from the National Research, Development and Innovation Office grants GINOP-2.3.2-15-2016-00020 TUMORDNS, GINOP-2.3.2-15-2016-00048-STAYALIVE and National Research Development and Innovation Office OTKA K132193, K147482. GH received funding from National Institutes of Health grants R01GM066189, R01DK113790 and R01HL158519. AB - Adenosine plays an important role in modulating immune cell function, particularly T cells and myeloid cells, such as macrophages and dendritic cells. Cell surface adenosine A2A receptors (A2AR) regulate the production of pro-inflammatory cytokines and chemokines, as well as the proliferation, differentiation, and migration of immune cells. In the present study, we expanded the A2AR interactome and provided evidence for the interaction between the receptor and the Niemann–Pick type C intracellular cholesterol transporter 1 (NPC1) protein. The NPC1 protein was identified to interact with the C-terminal tail of A2AR in RAW 264.7 and IPMФ cells by two independent and parallel proteomic approaches. The interaction between the NPC1 protein and the full-length A2AR was further validated in HEK-293 cells that permanently express the receptor and RAW264.7 cells that endogenously express A2AR. A2AR activation reduces the expression of NPC1 mRNA and protein density in LPS-activated mouse IPMФ cells. Additionally, stimulation of A2AR negatively regulates the cell surface expression of NPC1 in LPS-stimulated macrophages. Furthermore, stimulation of A2AR also altered the density of lysosome-associated membrane protein 2 (LAMP2) and early endosome antigen 1 (EEA1), two endosomal markers associated with the NPC1 protein. Collectively, these results suggested a putative A2AR-mediated regulation of NPC1 protein function in macrophages, potentially relevant for the Niemann–Pick type C disease when mutations in NPC1 protein result in the accumulation of cholesterol and other lipids in lysosomes. LA - English DB - MTMT ER - TY - BOOK AU - Gerencsér, A AU - Tóth, PÁ AU - Vígh, D AU - Kókai, Endre AU - Virág, László TI - Optimization of tumor cell killing by chimeric antigen receptor expressing macrophages PY - 2023 UR - https://m2.mtmt.hu/api/publication/33806508 ID - 33806508 LA - English DB - MTMT ER - TY - JOUR AU - Hajnády, Zoltán AU - Nagy-Pénzes, Máté AU - Demény, Máté Ágoston AU - Kovács, Katalin AU - El-Hamoly, Tarek AU - Maléth, József AU - Hegyi, Péter AU - Polgár, Zsuzsanna AU - Hegedűs, Csaba AU - Virág, László TI - OGG1 Inhibition Reduces Acinar Cell Injury in a Mouse Model of Acute Pancreatitis JF - BIOMEDICINES J2 - BIOMEDICINES VL - 10 PY - 2022 IS - 10 PG - 17 SN - 2227-9059 DO - 10.3390/biomedicines10102543 UR - https://m2.mtmt.hu/api/publication/33153168 ID - 33153168 N1 - * Megosztott szerzőség AB - Acute pancreatitis (AP) is a potentially life-threatening gastrointestinal disease with a complex pathology including oxidative stress. Oxidative stress triggers oxidative DNA lesions such as formation of 7,8-dihydro-8-oxo-2′-oxoguanine (8-oxoG) and also causes DNA strand breaks. DNA breaks can activate the nuclear enzyme poly(ADP-ribose) polymerase 1 (PARP1) which contributes to AP pathology. 8-oxoG is recognized by 8-oxoG glycosylase 1 (OGG1) resulting in the removal of 8-oxoG from DNA as an initial step of base excision repair. Since OGG1 also possesses a DNA nicking activity, OGG1 activation may also trigger PARP1 activation. In the present study we investigated the role played by OGG1 in AP. We found that the OGG1 inhibitor compound TH5487 reduced edema formation, inflammatory cell migration and necrosis in a cerulein-induced AP model in mice. Moreover, TH5487 caused 8-oxoG accumulation and reduced tissue poly(ADP-ribose) levels. Consistent with the indirect PARP inhibitory effect, TH5487 shifted necrotic cell death (LDH release and Sytox green uptake) towards apoptosis (caspase activity) in isolated pancreatic acinar cells. In the in vivo AP model, TH5487 treatment suppressed the expression of various cytokine and chemokine mRNAs such as those of TNF, IL-1β, IL1ra, IL6, IL16, IL23, CSF, CCL2, CCL4, CCL12, IL10 and TREM as measured with a cytokine array and verified by RT-qPCR. As a potential mechanism underlying the transcriptional inhibitory effect of the OGG1 inhibitor we showed that while 8-oxoG accumulation in the DNA facilitates NF-κB binding to its consensus sequence, when OGG1 is inhibited, target site occupancy of NF-κB is impaired. In summary, OGG1 inhibition provides protection from tissue injury in AP and these effects are likely due to interference with the PARP1 and NF-κB activation pathways. LA - English DB - MTMT ER - TY - JOUR AU - Virág, László TI - 100 éves a Debreceni Egyetem Orvosi Vegytani Intézete JF - GERUNDIUM: EGYETEMTÖRTÉNETI KÖZLEMÉNYEK J2 - GERUNDIUM VL - MMXXII PY - 2022 IS - XIII nr. 1-2 SP - 203 EP - 216 PG - 14 SN - 2061-5132 DO - 10.29116/gerundium/2022/1-2/13 UR - https://m2.mtmt.hu/api/publication/33140473 ID - 33140473 LA - Hungarian DB - MTMT ER - TY - JOUR AU - Nagy-Pénzes, Máté AU - Hajnády, Zoltán AU - Regdon, Zsolt AU - Demény, Máté Ágoston AU - Kovács, Katalin AU - El-Hamoly, Tarek AU - Maléth, József AU - Hegyi, Péter AU - Hegedűs, Csaba AU - Virág, László TI - Tricetin Reduces Inflammation and Acinar Cell Injury in Cerulein-Induced Acute Pancreatitis: The Role of Oxidative Stress-Induced DNA Damage Signaling JF - BIOMEDICINES J2 - BIOMEDICINES VL - 10 PY - 2022 IS - 6 PG - 20 SN - 2227-9059 DO - 10.3390/biomedicines10061371 UR - https://m2.mtmt.hu/api/publication/32886684 ID - 32886684 N1 - * Megosztott szerzőség LA - English DB - MTMT ER - TY - JOUR AU - Skopál, Adrienn AU - Kéki, T AU - Tóth, PÁ AU - Csóka, B AU - Koscsó, B AU - Német, ZH AU - Antonioli, L AU - Ivessa, A AU - Ciruela, F AU - Virág, László AU - Haskó, György AU - Kókai, Endre TI - Cathepsin D interacts with adenosine A2A receptors in mouse macrophages to modulate cell surface localization and inflammatory signalling JF - JOURNAL OF BIOLOGICAL CHEMISTRY J2 - J BIOL CHEM VL - 298 PY - 2022 IS - 5 PG - 18 SN - 0021-9258 DO - 10.1016/j.jbc.2022.101888 UR - https://m2.mtmt.hu/api/publication/32799560 ID - 32799560 N1 - Funding Agency and Grant Number: OTKA [MB08A 84685]; National Research, Development and Innovation Office [GINOP-2.3.2-15-2016-00020-TUMORDNS, GINOP-2.3.2-152016-00048-STAYALIVE, OTKA-K132193]; National Institutes of Health [R01GM066189, R01DK113790, R01HL158519, 1 R35 GM145245]; MCIN/AEI "ERDF. A way of making Europe" [PID2020-118511RB-I00] Funding text: E. K. received funding from OTKA (grant no.: MB08A 84685). L. V. received funding from the National Research, Development and Innovation Office grants (GINOP-2.3.2-15-2016-00020-TUMORDNS, GINOP-2.3.2-152016-00048-STAYALIVE, and OTKA-K132193). G. H. received funding from the National Institutes of Health grants R01GM066189, R01DK113790, R01HL158519, and 1 R35 GM145245. Also supported by project PID2020-118511RB-I00 founded by MCIN/AEI/10.13039/501100011033 "ERDF. A way of making Europe" to F. C. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. LA - English DB - MTMT ER -