@article{MTMT:32068433,
	title = {AIM2-driven inflammasome activation in heart failure},
	url = {https://m2.mtmt.hu/api/publication/32068433},
	author = {Onódi, Zsófia and Ruppert, Mihály and Kucsera, Dániel and Sayour, Alex Ali and Tóth, Viktória and Koncsos, Gábor and Novák, Julianna and Brenner, Gábor and Makkos, András and Baranyai, Tamás and Giricz, Zoltán and Görbe, Anikó and Leszek, Przemyslaw and Gyöngyösi, Mariann and Horváth, Iván and Schulz, Rainer and Merkely, Béla Péter and Ferdinandy, Péter and Radovits, Tamás and Varga, Zoltán},
	doi = {10.1093/cvr/cvab202},
	journal-iso = {CARDIOVASC RES},
	journal = {CARDIOVASCULAR RESEARCH},
	volume = {117},
	unique-id = {32068433},
	issn = {0008-6363},
	year = {2021},
	eissn = {1755-3245},
	pages = {2639-2651},
	orcid-numbers = {Onódi, Zsófia/0000-0002-3746-8016; Kucsera, Dániel/0000-0001-9446-847X; Sayour, Alex Ali/0000-0001-7728-4775; Tóth, Viktória/0000-0002-0426-2425; Koncsos, Gábor/0000-0001-5451-8719; Brenner, Gábor/0000-0001-7886-2960; Makkos, András/0000-0002-0309-4909; Baranyai, Tamás/0000-0002-9378-8938; Giricz, Zoltán/0000-0003-2036-8665; Görbe, Anikó/0000-0003-4908-1094; Merkely, Béla Péter/0000-0001-6514-0723; Ferdinandy, Péter/0000-0002-6424-6806; Varga, Zoltán/0000-0002-2758-0784}
}

@article{MTMT:31923243,
	title = {Balanced Intense Exercise Training Induces Atrial Oxidative Stress Counterbalanced by the Antioxidant System and Atrial Hypertrophy That Is Not Associated with Pathological Remodeling or Arrhythmogenicity},
	url = {https://m2.mtmt.hu/api/publication/31923243},
	author = {Oláh, Attila and Barta, Bálint András and Sayour, Alex Ali and Ruppert, Mihály and Virág-Tulassay, Eszter and Novák, Julianna and Varga, Zoltán and Ferdinandy, Péter and Merkely, Béla Péter and Radovits, Tamás},
	doi = {10.3390/antiox10030452},
	journal-iso = {ANTIOXIDANTS-BASEL},
	journal = {ANTIOXIDANTS},
	volume = {10},
	unique-id = {31923243},
	year = {2021},
	eissn = {2076-3921},
	orcid-numbers = {Sayour, Alex Ali/0000-0001-7728-4775; Virág-Tulassay, Eszter/0000-0001-7570-3016; Varga, Zoltán/0000-0002-2758-0784; Ferdinandy, Péter/0000-0002-6424-6806; Merkely, Béla Péter/0000-0001-6514-0723}
}

@article{MTMT:31348421,
	title = {Chronic treatment with rofecoxib but not ischemic preconditioning of the myocardium ameliorates early intestinal damage following cardiac ischemia/reperfusion injury in rats},
	url = {https://m2.mtmt.hu/api/publication/31348421},
	author = {László, Szilvia Bianka and Lázár, Bernadette and Brenner, Gábor and Makkos, András and Balogh, Mihály and Al-Khrasani, Mahmoud and Hutka, Barbara and Mohammadzadeh, Amir and Kemény, Ágnes and Horváthné László, Terézia and Scheich, Bálint and Szabados, Tamara and Kenyeres, Éva and Giricz, Zoltán and Bencsik, Péter and Varga, Zoltán and Novák, Julianna and Helyes, Zsuzsanna and Ferdinandy, Péter and Gyires, Klára and Zádori, Zoltán Sándor},
	doi = {10.1016/j.bcp.2020.114099},
	journal-iso = {BIOCHEMIC PHARMACOL},
	journal = {BIOCHEMICAL PHARMACOLOGY},
	volume = {178},
	unique-id = {31348421},
	issn = {0006-2952},
	abstract = {There is some recent evidence that cardiac ischemia/reperfusion (I/R) injury induces intestinal damage within days, which contributes to adverse cardiovascular outcomes after myocardial infarction. However, it is not clear whether remote gut injury has any detectable early signs, and whether different interventions aiming to reduce cardiac damage are also effective at protecting the intestine. Previously, we found that chronic treatment with rofecoxib, a selective inhibitor of cyclooxygenase-2 (COX-2), limited myocardial infarct size to a comparable extent as cardiac ischemic preconditioning (IPC) in rats subjected to 30-min coronary artery occlusion and 120-min reperfusion. In the present study, we aimed to analyse the early intestinal alterations caused by cardiac I/R injury, with or without the above-mentioned infart size-limiting interventions. We found that cardiac I/R injury induced histological changes in the small intestine within 2 hours, which were accompanied by elevated tissue level of COX-2 and showed positive correlation with the activity of matrix metalloproteinase-2 (MMP-2), but not of MMP-9 in the plasma. All these changes were prevented by rofecoxib treatment. By contrast, cardiac IPC failed to reduce intestinal injury and plasma MMP-2 activity, although it prevented the transient reduction in jejunal blood flow in response to cardiac I/R. Our results demonstrate for the first time that rapid development of intestinal damage follows cardiac I/R, and that two similarly effective infarct size-limiting interventions, rofecoxib treatment and cardiac IPC, have different impacts on cardiac I/R-induced gut injury. Furthermore, intestinal damage correlates with plasma MMP-2 activity, which may be a biomarker for its early diagnosis.},
	keywords = {CYCLOOXYGENASE-2; Ischemic Preconditioning; myocardial infarction; matrix metalloproteinase; Small intestine; Remote ischemia/reperfusion injury},
	year = {2020},
	eissn = {1873-2968},
	orcid-numbers = {László, Szilvia Bianka/0000-0001-9755-8972; Lázár, Bernadette/0000-0001-8123-8720; Brenner, Gábor/0000-0001-7886-2960; Makkos, András/0000-0002-0309-4909; Balogh, Mihály/0000-0003-3296-0316; Al-Khrasani, Mahmoud/0000-0001-8488-3266; Hutka, Barbara/0000-0002-7692-2744; Mohammadzadeh, Amir/0000-0001-6747-1913; Kemény, Ágnes/0000-0002-4523-3938; Horváthné László, Terézia/0000-0002-1635-0633; Szabados, Tamara/0000-0001-8920-1666; Kenyeres, Éva/0000-0002-6070-2560; Giricz, Zoltán/0000-0003-2036-8665; Bencsik, Péter/0000-0003-1936-6232; Varga, Zoltán/0000-0002-2758-0784; Ferdinandy, Péter/0000-0002-6424-6806; Gyires, Klára/0000-0002-4718-2345; Zádori, Zoltán Sándor/0000-0001-7312-618X}
}

@article{MTMT:3040958,
	title = {Novel role for galectin-1 in T-cell apoptosis regulation and ist relevance to systemic lupus erythematosus},
	url = {https://m2.mtmt.hu/api/publication/3040958},
	author = {Hornung, Ákos and Deák, Magdolna and Novák, Julianna and E, Szabó and A, Czibula and R, Fajka-Boja and Kriston-Pál, Éva and Monostori, É and Kovács, László},
	doi = {10.1136/annrheumdis-2015-207259.44},
	journal-iso = {ANN RHEUM DIS},
	journal = {ANNALS OF THE RHEUMATIC DISEASES},
	volume = {74},
	unique-id = {3040958},
	issn = {0003-4967},
	year = {2015},
	eissn = {1468-2060},
	pages = {A19-A19},
	orcid-numbers = {Kovács, László/0000-0003-4457-1430}
}

@article{MTMT:2807186,
	title = {Novel role for galectin-1 in T-cells under physiological and pathological conditions},
	url = {https://m2.mtmt.hu/api/publication/2807186},
	author = {Deák, Magdolna and Hornung, Ákos and Novák, Julianna and Demydenko, Dmytro and Szabó, Enikő and Czibula, Ágnes and Fajka-Boja, Roberta and Kriston-Pál, Éva and Monostori, Éva and Kovács, László},
	doi = {10.1016/j.imbio.2014.10.023},
	journal-iso = {IMMUNOBIOLOGY},
	journal = {IMMUNOBIOLOGY},
	volume = {220},
	unique-id = {2807186},
	issn = {0171-2985},
	abstract = {Secreted, extracellular galectin-1 (exGal-1) but not intracellular Gal-1 (inGal-1) has been described as a strong immunosuppressive protein due to its major activity of inducing apoptosis of activated T-cells. It has previously been reported that T-cells express Gal-1 upon activation, however its participation in T-cell functions has remained largely elusive. To determine function of Gal-1 expressed by activated T-cells we have carried out a series of experiments. We have shown that Gal-1, expressed in Gal-1-transgenic Jurkat cells or in activated T-cells, remained intracellularly indicating that Gal-1-induced T-cell death was not a result of an autocrine effect of the de novo expressed Gal-1. Rather, a particular consequence of the inGal-1 expression was that T-cells became more sensitive to exGal-1 added either as a soluble protein or bound to the surface of a Gal-1-secreting effector cell. This was also verified when the susceptibility of activated T-cells from wild type or Gal-1 knockout mice to Gal-1-induced apoptosis were compared. Murine T-cells expressing Gal-1 were more sensitive to the cytotoxicity of the exGal-1 than their Gal-1 knockout counterparts. We also conducted a study with activated T-cells from patients with systemic lupus erythematosus (SLE), a disease in which dysregulated T-cell apoptosis has been well described. SLE T-cells expressed lower amounts of Gal-1 than healthy T-cells and were less sensitive to exGal-1. These results suggested a novel role of inGal-1 in T-cells as a regulator of T-cell response to exGal-1, and its likely contribution to the mechanism in T-cell apoptosis deficiency in lupus.},
	year = {2015},
	eissn = {1878-3279},
	pages = {483-489},
	orcid-numbers = {Czibula, Ágnes/0000-0003-4461-2773; Fajka-Boja, Roberta/0000-0001-5331-8280; Monostori, Éva/0000-0002-7442-3562; Kovács, László/0000-0003-4457-1430}
}

@article{MTMT:2459241,
	title = {GM1 controlled lateral segregation of tyrosine kinase Lck predispose T-cells to cell-derived galectin-1-induced apoptosis.},
	url = {https://m2.mtmt.hu/api/publication/2459241},
	author = {Novák, Julianna and Kriston-Pál, Éva and Czibula, Ágnes and Deák, Magdolna and Kovács, László and Monostori, Éva and Fajka-Boja, Roberta},
	doi = {10.1016/j.molimm.2013.10.010},
	journal-iso = {MOL IMMUNOL},
	journal = {MOLECULAR IMMUNOLOGY},
	volume = {57},
	unique-id = {2459241},
	issn = {0161-5890},
	abstract = {One prominent immunoregulatory function of galectin-1 (Gal-1), a beta-galactoside binding mammalian lectin, is induction of apoptosis in activated T-cells by a process depending on the activity of Src family tyrosine kinase, Lck. Although the requirement for Lck in Gal-1 induced T-cell death and the ability of Gal-1 to affect the membrane localization of extracellular Gal-1-binding proteins have been well documented, the consequence of the complex and related reorganization of extra- and intracellular signaling components upon Gal-1 treatment of T-cells has not yet been revealed. Therefore, we have analyzed the plasma membrane movement of Lck upon Gal-1 triggered signaling, and the significance of this event in Gal-1 induced T-cell death. Non-receptor tyrosine kinase, Lck primarily localized in the synapse of tumor cell-T-cell during 15min of the established direct cell contact. Later, after 30min, a lateral segregation of Lck from the cell synapse was observed. The migration of Lck to the opposite of the cell contact apparently depended on the expression and cell surface presentation of Gal-1 on the effector (tumor) cells and was accompanied by phosphorylation on the negative regulatory tyrosine residue, Tyr505. Receptor tyrosine phosphatase, CD45 played crucial role in this event since CD45 deficiency or inhibition of its phosphatase activity resulted in the failure of Lck membrane movement. Level of the Gal-1-binding glycolipid GM1 ganglioside also essentially regulated Lck localization. Segregation of Lck and Gal-1 induced apoptosis was diminished in T-cells with low GM1 expression compared to T-cells with high GM1. Our results show that spatial regulation of Lck by CD45 and GM1 ganglioside determines the outcome of apoptotic response to Gal-1 and this local regulation may occur only upon intimate effector (Gal-1 expressing) cell-T-cell attachment.},
	year = {2014},
	eissn = {1872-9142},
	pages = {302-309},
	orcid-numbers = {Czibula, Ágnes/0000-0003-4461-2773; Kovács, László/0000-0003-4457-1430; Monostori, Éva/0000-0002-7442-3562; Fajka-Boja, Roberta/0000-0001-5331-8280}
}

@article{MTMT:2601975,
	title = {Galectin-1 and immunoregulatory dysfunction in systemic lupus erythematosus},
	url = {https://m2.mtmt.hu/api/publication/2601975},
	author = {Deák, Magdolna and Novák, Julianna and Czibula, A and Fajka-Boja, R and Monostori, E and Kovács, László},
	journal-iso = {EUR J CLIN INVEST},
	journal = {EUROPEAN JOURNAL OF CLINICAL INVESTIGATION},
	volume = {43},
	unique-id = {2601975},
	issn = {0014-2972},
	year = {2013},
	eissn = {1365-2362},
	pages = {86-86},
	orcid-numbers = {Kovács, László/0000-0003-4457-1430}
}

@article{MTMT:2057717,
	title = {Identification of Galectin-1 as a Critical Factor in Function of Mouse Mesenchymal Stromal Cell-Mediated Tumor Promotion},
	url = {https://m2.mtmt.hu/api/publication/2057717},
	author = {Szebeni, Gábor and Kriston-Pál, Éva and Blazsó, Péter and Katona, Róbert László and Novák, Julianna and Szabó, Enikő and Czibula, Ágnes and Fajka-Boja, Roberta and Hegyi, Beáta and Uher, Ferenc and Krenács, László and Joó, Gabriella and Monostori, Éva},
	doi = {10.1371/journal.pone.0041372},
	journal-iso = {PLOS ONE},
	journal = {PLOS ONE},
	volume = {7},
	unique-id = {2057717},
	issn = {1932-6203},
	abstract = {Bone marrow derived mesenchymal stromal cells (MSCs) have recently been implicated as one source of the tumor-associated stroma, which plays essential role in regulating tumor progression. In spite of the intensive research, the individual factors in MSCs controlling tumor progression have not been adequately defined. In the present study we have examined the role of galectin-1 (Gal-1), a protein highly expressed in tumors with poor prognosis, in MSCs in the course of tumor development. Co-transplantation of wild type MSCs with 4T1 mouse breast carcinoma cells enhances the incidence of palpable tumors, growth, vascularization and metastasis. It also reduces survival compared to animals treated with tumor cells alone or in combination with Gal-1 knockout MSCs. In vitro studies show that the absence of Gal-1 in MSCs does not affect the number of migrating MSCs toward the tumor cells, which is supported by the in vivo migration of intravenously injected MSCs into the tumor. Moreover, differentiation of endothelial cells into blood vessel-like structures strongly depends on the expression of Gal-1 in MSCs. Vital role of Gal-1 in MSCs has been further verified in Gal-1 knockout mice. By administering B16F10 melanoma cells into Gal-1 deficient animals, tumor growth is highly reduced compared to wild type animals. Nevertheless, co-injection of wild type but not Gal-1 deficient MSCs results in dramatic tumor growth and development. These results confirm that galectin-1 is one of the critical factors in MSCs regulating tumor progression.},
	year = {2012},
	eissn = {1932-6203},
	orcid-numbers = {Szebeni, Gábor/0000-0002-6998-5632; Blazsó, Péter/0000-0003-4404-8068; Czibula, Ágnes/0000-0003-4461-2773; Fajka-Boja, Roberta/0000-0001-5331-8280; Uher, Ferenc/0000-0001-7997-6142; Krenács, László/0000-0001-6541-3031; Joó, Gabriella/0000-0001-5900-838X; Monostori, Éva/0000-0002-7442-3562}
}

@article{MTMT:1303865,
	title = {Mechanism of tumor cell-induced T-cell apoptosis mediated by galectin-1},
	url = {https://m2.mtmt.hu/api/publication/1303865},
	author = {Kovács, Ferenc and Blaskó, Andrea and Fajka-Boja, Roberta and Katona, Róbert László and Végh, Lea and Novák, Julianna and Szebeni, Gábor and Krenács, László and Uher, Ferenc and Tubak, Vilmos and Kiss, R and Monostori, Éva},
	doi = {10.1016/j.imlet.2009.10.003},
	journal-iso = {IMMUNOL LETT},
	journal = {IMMUNOLOGY LETTERS},
	volume = {127},
	unique-id = {1303865},
	issn = {0165-2478},
	abstract = {Galectin-1 (Gal-1) has been implicated in tumor progression partly via the induction of T-cell apoptosis. However the mechanism of Gal-1 induced T-cell death was mostly studied using recombinant, soluble Gal-1 producing controversial results. To explore the true mechanism of Gal-1 and hence tumor cell-induced T-cell death, we applied co-cultures of tumor cells and T-cells thus avoiding artificial circumstances generated using recombinant protein. T-cells died when co-cultured with Gal-1-expressing but survived with Gal-1 non-expressing tumor cells. Removing tumor cell surface Gal-1 or knocking down Gal-1 expression resulted in diminution of T-cell apoptosis. Gal-1 transgenic or soluble Gal-1 treated HeLa cells became cytotoxic. Stimulation of apoptosis required interaction between the tumor and T-cells, presence of p56lck and ZAP70, decrease of mitochondrial membrane potential and caspase activation. Hence tumor cell-derived Gal-1 might efficiently contribute to tumor self-defense. Moreover this system resolves the discrepancies obtained using recombinant Gal-1 in T-cell apoptosis studies. © 2009 Elsevier B.V. All rights reserved.},
	keywords = {Tumor-associated stroma cells; Tumor cells; T-cell apoptosis; Galectin-1},
	year = {2010},
	eissn = {1879-0542},
	pages = {108-118},
	orcid-numbers = {Fajka-Boja, Roberta/0000-0001-5331-8280; Szebeni, Gábor/0000-0002-6998-5632; Krenács, László/0000-0001-6541-3031; Uher, Ferenc/0000-0001-7997-6142; Tubak, Vilmos/0000-0002-6141-3920; Monostori, Éva/0000-0002-7442-3562}
}

@article{MTMT:3062016,
	title = {Mechanism of T-cell death induced by tumor cell-derived galectin-1, that acts via direct cell-cell contact},
	url = {https://m2.mtmt.hu/api/publication/3062016},
	author = {Fajka-Boja, R and Kovacs-Solyom, F and Katona, RL and Szebeni, Gábor and Krenacs, L and Vegh, L and Blasko, A and Uher, F and Novák, Julianna and Tubak, V and Kiss, E and Monostori, E},
	journal-iso = {EUR J IMMUNOL},
	journal = {EUROPEAN JOURNAL OF IMMUNOLOGY},
	volume = {39},
	unique-id = {3062016},
	issn = {0014-2980},
	year = {2009},
	eissn = {1521-4141},
	pages = {S195},
	orcid-numbers = {Szebeni, Gábor/0000-0002-6998-5632}
}