@article{MTMT:34735575, title = {P2X7 receptor inhibition alleviates mania-like behavior independently of interleukin-1β}, url = {https://m2.mtmt.hu/api/publication/34735575}, author = {Gölöncsér, Flóra and Baranyi, Mária and Tod, Pál and Maácz, Fruzsina and Sperlágh, Beáta}, doi = {10.1016/j.isci.2024.109284}, journal-iso = {ISCIENCE}, journal = {ISCIENCE}, volume = {27}, unique-id = {34735575}, year = {2024}, eissn = {2589-0042}, orcid-numbers = {Tod, Pál/0000-0001-9163-7071} } @article{MTMT:34206800, title = {The antidepressant effect of short- and long-term zinc exposition is partly mediated by P2X7 receptors in male mice}, url = {https://m2.mtmt.hu/api/publication/34206800}, author = {Varga, Bernadett and Baranyi, Mária and Gölöncsér, Flóra and Tod, Pál and Sperlágh, Beáta}, doi = {10.3389/fphar.2023.1241406}, journal-iso = {FRONT PHARMACOL}, journal = {FRONTIERS IN PHARMACOLOGY}, volume = {14}, unique-id = {34206800}, abstract = {Background: As a member of the purinergic receptor family, divalent cation-regulated ionotropic P2X7 (P2rx7) plays a role in the pathophysiology of psychiatric disorders. This study aimed to investigate whether the effects of acute zinc administration and long-term zinc deprivation on depression-like behaviors in mice are mediated by P2X7 receptors.}, keywords = {BEHAVIOR; DEPRESSION; ZINC; purinergic receptor; P2X7}, year = {2023}, eissn = {1663-9812}, orcid-numbers = {Varga, Bernadett/0000-0001-8753-861X; Tod, Pál/0000-0001-9163-7071} } @article{MTMT:33642580, title = {Dual Role of the P2X7 Receptor in Dendritic Outgrowth during Physiological and Pathological Brain Development.}, url = {https://m2.mtmt.hu/api/publication/33642580}, author = {Mut-Arbona, Paula and Huang, Lumei and Baranyi, Mária and Tod, Pál and Iring, András and Calzaferri, Francesco and de los Ríos, Cristobal and Sperlágh, Beáta}, doi = {10.1523/JNEUROSCI.0805-22.2022}, journal-iso = {J NEUROSCI}, journal = {JOURNAL OF NEUROSCIENCE}, volume = {43}, unique-id = {33642580}, issn = {0270-6474}, abstract = {At high levels, extracellular ATP operates as a “danger” molecule under pathologic conditions through purinergic receptors, including the ionotropic P2X7 receptor (P2X7R). Its endogenous activation is associated with neurodevelopmental disorders; however, its function during early embryonic stages remains largely unclear. Our objective was to determine the role of P2X7R in the regulation of neuronal outgrowth. For this purpose, we performed Sholl analysis of dendritic branches on primary hippocampal neurons and in acute hippocampal slices from WT mice and mice with genetic deficiency or pharmacological blockade of P2X7R. Because abnormal dendritic branching is a hallmark of certain neurodevelopmental disorders, such as schizophrenia, a model of maternal immune activation (MIA)-induced schizophrenia, was used for further morphologic investigations. Subsequently, we studied MIA-induced behavioral deficits in young adult mice females and males. Genetic deficiency or pharmacological blockade of P2X7R led to branching deficits under physiological conditions. Moreover, pathologic activation of the receptor led to deficits in dendritic outgrowth on primary neurons from WT mice but not those from P2X7R KO mice exposed to MIA. Likewise, only MIA-exposed WT mice displayed schizophrenia-like behavioral and cognitive deficits. Therefore, we conclude that P2X7R has different roles in the development of hippocampal dendritic arborization under physiological and pathologic conditions.}, keywords = {SCHIZOPHRENIA; BEHAVIOR; ATP; Dendrites; P2X7; Sholl analysis}, year = {2023}, eissn = {1529-2401}, pages = {1125-1142}, orcid-numbers = {Mut-Arbona, Paula/0000-0002-3804-3140; Tod, Pál/0000-0001-9163-7071; Iring, András/0000-0002-3087-4337; Calzaferri, Francesco/0000-0002-4781-2925} } @mastersthesis{MTMT:32851632, title = {Functional recovery of the post-ischemic kidney after delayed contralateral nephrectomy: Pivotal role of inflammation and miRNAs}, url = {https://m2.mtmt.hu/api/publication/32851632}, author = {Tod, Pál}, doi = {10.14753/SE.2022.2613}, unique-id = {32851632}, year = {2022}, orcid-numbers = {Tod, Pál/0000-0001-9163-7071} } @article{MTMT:32791102, title = {Elevated serum purine levels in schizophrenia: a reverse translational study to identify novel inflammatory biomarkers}, url = {https://m2.mtmt.hu/api/publication/32791102}, author = {Kristóf, Zsüliet and Baranyi, Mária and Tod, Pál and Mut-Arbona, Paula and Demeter, Kornél and Bitter, István and Sperlágh, Beáta}, doi = {10.1093/ijnp/pyac026}, journal-iso = {INT J NEUROPSYCHOPH}, journal = {INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY}, volume = {25}, unique-id = {32791102}, issn = {1461-1457}, year = {2022}, eissn = {1469-5111}, pages = {645-659}, orcid-numbers = {Tod, Pál/0000-0001-9163-7071; Mut-Arbona, Paula/0000-0002-3804-3140; Bitter, István/0000-0002-9464-4709} } @article{MTMT:32624327, title = {Maternal P2X7 receptor inhibition prevents autism-like phenotype in male mouse offspring through the NLRP3-IL-1β pathway.}, url = {https://m2.mtmt.hu/api/publication/32624327}, author = {Szabó, Dorottya and Tod, Pál and Gölöncsér, Flóra and Román, Viktor and Lendvai, Balázs and Bereczkiné Otrokocsi, Lilla and Sperlágh, Beáta}, doi = {10.1016/j.bbi.2022.01.015}, journal-iso = {BRAIN BEHAV IMMUN}, journal = {BRAIN BEHAVIOR AND IMMUNITY}, volume = {101}, unique-id = {32624327}, issn = {0889-1591}, abstract = {Autism spectrum disorder (ASD) is a complex neurodevelopmental condition caused by interactions of environmental and genetic factors. Recently we showed that activation of the purinergic P2X7 receptors is necessary and sufficient to convert maternal immune activation (MIA) to ASD-like features in male offspring mice. Our aim was to further substantiate these findings and identify downstream signaling pathways coupled to P2X7 upon MIA. Maternal treatment with the NLRP3 antagonist MCC950 and a neutralising IL-1β antibody during pregnancy counteracted the development of autistic characteristics in offspring mice. We also explored time-dependent changes of a widespread cytokine and chemokine profile in maternal blood and fetal brain samples of poly(I:C)/saline-treated dams. MIA-induced increases in plasma IL-1β, RANTES, MCP-1, and fetal brain IL-1β, IL-2, IL-6, MCP-1 concentrations are regulated by the P2X7/NLRP3 pathway. Offspring treatment with the selective P2X7 receptor antagonist JNJ47965567 was effective in the prevention of autism-like behavior in mice using a repeated dosing protocol. Our results highlight that in addition to P2X7, NLRP3, as well as inflammatory cytokines, may also be potential biomarkers and therapeutic targets of social deficits and repetitive behaviors observed in autism spectrum disorder.}, keywords = {BEHAVIOR; INFECTION; Cytokines; neuroinflammation; P2X7; neurodevelopment; Maternal immune activation; poly(I:C); Autism}, year = {2022}, eissn = {1090-2139}, pages = {318-332}, orcid-numbers = {Szabó, Dorottya/0000-0002-8301-6299; Tod, Pál/0000-0001-9163-7071} } @article{MTMT:32470555, title = {Divergent regulation of lncRNA expression by ischemia in adult and aging mice.}, url = {https://m2.mtmt.hu/api/publication/32470555}, author = {Kaucsár, Tamás and Róka, Beáta and Tod, Pál and Do, Thanh Phuong and Hegedűs, Zoltán and Szénási, Gábor and Hamar, Péter}, doi = {10.1007/s11357-021-00460-9}, journal-iso = {GEROSCIENCE}, journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)}, volume = {44}, unique-id = {32470555}, issn = {2509-2715}, abstract = {Elderly patients have increased susceptibility to acute kidney injury (AKI). Long noncoding RNAs (lncRNA) are key regulators of cellular processes, and have been implicated in both aging and AKI. Our aim was to study the effects of aging and ischemia-reperfusion injury (IRI) on the renal expression of lncRNAs. Adult and old (10- and 26-30-month-old) C57BL/6 N mice were subjected to unilateral IRI followed by 7 days of reperfusion. Renal expression of 90 lncRNAs and mRNA expression of injury, regeneration, and fibrosis markers was measured by qPCR in the injured and contralateral control kidneys. Tubular injury, regeneration, and fibrosis were assessed by histology. Urinary lipocalin-2 excretion was increased in old mice prior to IRI, but plasma urea was similar. In the control kidneys of old mice tubular cell necrosis and apoptosis, mRNA expression of kidney injury molecule-1, fibronectin-1, p16, and p21 was elevated. IRI increased plasma urea concentration only in old mice, but injury, regeneration, and fibrosis scores and their mRNA markers were similar in both age groups. AK082072 and Y lncRNAs were upregulated, while H19 and RepA transcript were downregulated in the control kidneys of old mice. IRI upregulated Miat, Igf2as, SNHG5, SNHG6, RNCR3, Malat1, Air, Linc1633, and Neat1 v1, while downregulated Linc1242. LncRNAs H19, AK082072, RepA transcript, and Six3os were influenced by both aging and IRI. Our results indicate that both aging and IRI alter renal lncRNA expression suggesting that lncRNAs have a versatile and complex role in aging and kidney injury. An Ingenuity Pathway Analysis highlighted that the most downregulated H19 may be linked to aging/senescence through p53.}, keywords = {Ischemia-reperfusion injury; acute kidney injury; LncRNA}, year = {2022}, eissn = {2509-2723}, pages = {429-445}, orcid-numbers = {Kaucsár, Tamás/0000-0003-4460-1265; Róka, Beáta/0000-0002-1491-1644; Tod, Pál/0000-0001-9163-7071; Szénási, Gábor/0000-0002-7350-6091; Hamar, Péter/0000-0002-1095-3564} } @article{MTMT:32153531, title = {Initial Renal Function (eGFR) Is a Prognostic Marker of Severe Acute Pancreatitis: A Cohort-Analysis of 1,224 Prospectively Collected Cases}, url = {https://m2.mtmt.hu/api/publication/32153531}, author = {Tod, Pál and Borbásné Farkas, Kornélia and Németh, Dávid and Szénási, Gábor and Vincze, Áron and Hágendorn, Roland and Czakó, László and Illés, Dóra and Izbéki, Ferenc and Dunás-Varga, Veronika and Papp, Mária and Hamvas, József and Varga, Márta and Gombos, Katalin and Nagy, Tamás and Márton, Zsolt and Faluhelyi, Nándor and Török, Imola and Ince, Ali Tüzün and Galeev, Shamil and Hegyi, Péter Jenő and Szentesi, Andrea Ildikó and Párniczky, Andrea and Szakács, Zsolt and Hegyi, Péter and Hamar, Péter}, doi = {10.3389/fmed.2021.671917}, journal-iso = {FRONT MED}, journal = {FRONTIERS IN MEDICINE}, volume = {8}, unique-id = {32153531}, year = {2021}, eissn = {2296-858X}, orcid-numbers = {Tod, Pál/0000-0001-9163-7071; Borbásné Farkas, Kornélia/0000-0002-5349-6527; Szénási, Gábor/0000-0002-7350-6091; Vincze, Áron/0000-0003-2217-7686; Czakó, László/0000-0002-6331-0802; Izbéki, Ferenc/0000-0001-7767-4319; Papp, Mária/0000-0003-3662-4010; Nagy, Tamás/0000-0001-5437-1411; Szentesi, Andrea Ildikó/0000-0003-2097-6927; Szakács, Zsolt/0000-0002-7035-941X; Hegyi, Péter/0000-0003-0399-7259; Hamar, Péter/0000-0002-1095-3564} } @article{MTMT:32122064, title = {Delayed Contralateral Nephrectomy Halted Post-Ischemic Renal Fibrosis Progression and Inhibited the Ischemia-Induced Fibromir Upregulation in Mice}, url = {https://m2.mtmt.hu/api/publication/32122064}, author = {Róka, Beáta and Tod, Pál and Kaucsár, Tamás and Bukosza, Éva Nóra and Vörös, Imre and Varga, Zoltán and Petrovich, Balázs and Ágg, Bence and Ferdinandy, Péter and Szénási, Gábor and Hamar, Péter}, doi = {10.3390/biomedicines9070815}, journal-iso = {BIOMEDICINES}, journal = {BIOMEDICINES}, volume = {9}, unique-id = {32122064}, year = {2021}, eissn = {2227-9059}, orcid-numbers = {Róka, Beáta/0000-0002-1491-1644; Tod, Pál/0000-0001-9163-7071; Kaucsár, Tamás/0000-0003-4460-1265; Bukosza, Éva Nóra/0000-0001-7606-7824; Vörös, Imre/0000-0001-5922-6109; Varga, Zoltán/0000-0002-2758-0784; Petrovich, Balázs/0000-0002-9745-0416; Ágg, Bence/0000-0002-6492-0426; Ferdinandy, Péter/0000-0002-6424-6806; Szénási, Gábor/0000-0002-7350-6091; Hamar, Péter/0000-0002-1095-3564} } @article{MTMT:31797383, title = {Cold Saline Perfusion before Ischemia-Reperfusion Is Harmful to the Kidney and Is Associated with the Loss of Ezrin, a Cytoskeletal Protein, in Rats}, url = {https://m2.mtmt.hu/api/publication/31797383}, author = {Révész, Csaba and Wasik, Anita A. and Godó, Mária and Tod, Pál and Lehtonen, Sanna and Szénási, Gábor and Hamar, Péter}, doi = {10.3390/biomedicines9010030}, journal-iso = {BIOMEDICINES}, journal = {BIOMEDICINES}, volume = {9}, unique-id = {31797383}, year = {2021}, eissn = {2227-9059}, orcid-numbers = {Révész, Csaba/0000-0001-6016-526X; Tod, Pál/0000-0001-9163-7071; Szénási, Gábor/0000-0002-7350-6091; Hamar, Péter/0000-0002-1095-3564} }