TY - JOUR AU - Dinh, Hoa AU - Kovács, Zsuzsanna AU - Kis, Merse AU - Kupecz, Klaudia AU - Sejben, Anita AU - Szűcs, Gergő AU - Márványkövi, Fanni AU - Siska, Andrea AU - Freiwan, Marah AU - Pósa, Szonja Polett AU - Galla, Zsolt AU - Ibos, Katalin Eszter AU - Bodnár, Éva AU - Lauber, Gülsüm Yilmaz AU - Goncalves, Ana Isabel Antunes AU - Acar, Eylem AU - Kriston, András AU - Kovács, Ferenc AU - Horváth, Péter AU - Bozsó, Zsolt AU - Tóth, Gábor AU - Földesi, Imre AU - Monostori, Péter AU - Cserni, Gábor AU - Podesser, Bruno K. AU - Lehoczki, Andrea Marianna AU - Pokreisz, Peter AU - Kiss, Attila AU - Dux, László AU - Csabafi, Krisztina AU - Sárközy, Márta TI - Role of the kisspeptin-KISS1R axis in the pathogenesis of chronic kidney disease and uremic cardiomyopathy JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE VL - 46 PY - 2024 IS - 2 SP - 2463 EP - 2488 PG - 26 SN - 2509-2715 DO - 10.1007/s11357-023-01017-8 UR - https://m2.mtmt.hu/api/publication/34395398 ID - 34395398 N1 - Department of Biochemistry and Interdisciplinary Centre of Excellence, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary Department of Biochemistry, Bach Mai Hospital, Hanoi, 100000, Viet Nam Department of Pathophysiology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary Department of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary Department of Laboratory Medicine, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary Metabolic and Newborn Screening Laboratory, Department of Pediatrics, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary Ludwig Boltzmann Institute for Cardiovascular Research at Center for Biomedical Research and Translational Surgery, Medical University of Vienna, Vienna, 1090, Austria Synthetic and Systems Biology Unit, Biological Research Centre, Eötvös Loránd Research Network, Szeged, 6726, Hungary Single-Cell Technologies Ltd, Szeged, 6726, Hungary Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, 00014, Finland Department of Medical Chemistry, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary Departments of Hematology and Stem Cell Transplantation, South Pest Central Hospital, National Institute of Hematology and Infectious Diseases, Saint Ladislaus Campus, Budapest, Hungary Export Date: 16 April 2024 Correspondence Address: Dux, L.; Department of Biochemistry and Interdisciplinary Centre of Excellence, Hungary; email: dux.laszlo@med.u-szeged.hu Correspondence Address: Sárközy, M.; Department of Biochemistry and Interdisciplinary Centre of Excellence, Hungary; email: martasarkozy@gmail.com AB - The prevalence of chronic kidney disease (CKD) is increasing globally, especially in elderly patients. Uremic cardiomyopathy is a common cardiovascular complication of CKD, characterized by left ventricular hypertrophy (LVH), diastolic dysfunction, and fibrosis. Kisspeptins and their receptor, KISS1R, exert a pivotal influence on kidney pathophysiology and modulate age-related pathologies across various organ systems. KISS1R agonists, including kisspeptin-13 (KP-13), hold promise as novel therapeutic agents within age-related biological processes and kidney-related disorders. Our investigation aimed to elucidate the impact of KP-13 on the trajectory of CKD and uremic cardiomyopathy. Male Wistar rats (300–350 g) were randomized into four groups: (I) sham-operated, (II) 5/6 nephrectomy-induced CKD, (III) CKD subjected to a low dose of KP-13 (intraperitoneal 13 µg/day), and (IV) CKD treated with a higher KP-13 dose (intraperitoneal 26 µg/day). Treatments were administered daily from week 3 for 10 days. After 13 weeks, KP-13 increased systemic blood pressure, accentuating diastolic dysfunction’s echocardiographic indicators and intensifying CKD-associated markers such as serum urea levels, glomerular hypertrophy, and tubular dilation. Notably, KP-13 did not exacerbate circulatory uremic toxin levels, renal inflammation, or fibrosis markers. In contrast, the higher KP-13 dose correlated with reduced posterior and anterior wall thickness, coupled with diminished cardiomyocyte cross-sectional areas and concurrent elevation of inflammatory ( Il6, Tnf ), fibrosis ( Col1 ), and apoptosis markers ( Bax/Bcl2 ) relative to the CKD group. In summary, KP-13’s influence on CKD and uremic cardiomyopathy encompassed heightened blood pressure and potentially activated inflammatory and apoptotic pathways in the left ventricle. LA - English DB - MTMT ER - TY - JOUR AU - Letoha, Annamária AU - Hudák, Anett AU - Bozsó, Zsolt AU - Vizler, Csaba AU - Veres, Gábor AU - Szilák, László AU - Letoha, Tamás TI - The Nuclear Localization Signal of NF-κB p50 Enters the Cells via Syndecan-Mediated Endocytosis and Inhibits NF-κB Activity JF - INTERNATIONAL JOURNAL OF PEPTIDE RESEARCH AND THERAPEUTICS J2 - INT J PEPT RES THER VL - 29 PY - 2023 IS - 5 PG - 16 SN - 1573-3149 DO - 10.1007/s10989-023-10548-9 UR - https://m2.mtmt.hu/api/publication/34050718 ID - 34050718 AB - It is well established that cationic peptides can enter cells following attachment to polyanionic membrane components. We report that the basic nuclear localization signal (NLS) of the NF-κB p50 subunit is internalized via lipid raft-dependent endocytosis mediated by heparan sulfate proteoglycans and exerts significant NF-κB inhibitory activities both in vitro and in vivo. In vitro uptake experiments revealed that the p50 NLS peptide (CYVQRKRQKLMP) enters the cytoplasm and accumulates in the nucleus at 37 °C. Depleting cellular ATP pools or decreasing temperature to 4 °C abolished peptide internalization, confirming the active, energy-dependent endocytic uptake. Co-incubation with heparan sulfate or replacing the peptide’s basic residues with glycines markedly reduced the intracellular entry of the p50 NLS, referring to the role of polyanionic cell-surface proteoglycans in internalization. Furthermore, treatment with methyl-β-cyclodextrin greatly inhibited the peptide’s membrane translocation. Overexpression of the isoforms of the syndecan family of transmembrane proteoglycans, especially syndecan-4, increased the cellular internalization of the NLS, suggesting syndecans’ involvement in the peptide’s cellular uptake. In vitro , p50 NLS reduced NF-κB activity in TNF-α-induced L929 fibroblasts and LPS-stimulated RAW 264.7 macrophages. TNF-α-induced ICAM-1 expression of HMEC-1 human endothelial cells could also be inhibited by the peptide. Fifteen minutes after its intraperitoneal injection, the peptide rapidly entered the cells of the pancreas, an organ with marked syndecan-4 expression. In an acute pancreatitis model, an inflammatory disorder triggered by the activation of stress-responsive transcription factors like NF-κB, administration of the p50 NLS peptide reduced the severity of pancreatic inflammation by blocking NF-κB transcription activity and ameliorating the examined laboratory and histological markers of pancreatitis. LA - English DB - MTMT ER - TY - JOUR AU - Borbély, Emőke AU - Varga, Viktória AU - Szögi, Titanilla AU - Schuster, Ildikó AU - Bozsó, Zsolt AU - Penke, Botond AU - Fülöp, Lívia TI - Impact of Two Neuronal Sigma-1 Receptor Modulators, PRE084 and DMT, on Neurogenesis and Neuroinflammation in an Aβ1–42-Injected, Wild-Type Mouse Model of AD JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 23 PY - 2022 IS - 5 PG - 20 SN - 1661-6596 DO - 10.3390/ijms23052514 UR - https://m2.mtmt.hu/api/publication/32753550 ID - 32753550 N1 - Funding Agency and Grant Number: National Research, Development, and Innovation Office [GINOP-2.3.2-15-2016-00060]; Hungarian Brain Research Program I [KTIA_13_NAP-A-III/7, 2017-1.2.1-NKP-2017-00002]; Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund [TKP2021EGA-32]; Hungarian Brain Research Program II [KTIA_13_NAP-A-III/7, 2017-1.2.1-NKP-2017-00002] Funding text: This project was supported by the National Research, Development, and Innovation Office (GINOP-2.3.2-15-2016-00060) and by the Hungarian Brain Research Program I and II-Grant No. KTIA_13_NAP-A-III/7, and 2017-1.2.1-NKP-2017-00002. Support by the Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund (TKP2021EGA-32) is acknowledged. LA - English DB - MTMT ER - TY - JOUR AU - Datki, Zsolt László AU - Balázs, Evelin AU - Gálik, Bence AU - Sinka, Rita AU - Zeitler, Lavínia AU - Bozsó, Zsolt AU - Kálmán, János AU - Hortobágyi, Tibor AU - Oláh, Zita TI - The interacting rotifer-biopolymers are anti- and disaggregating agents for human-type beta-amyloid in vitro JF - INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES J2 - INT J BIOL MACROMOL VL - 201 PY - 2022 SP - 262 EP - 269 PG - 8 SN - 0141-8130 DO - 10.1016/j.ijbiomac.2021.12.184 UR - https://m2.mtmt.hu/api/publication/32591465 ID - 32591465 N1 - Funding Agency and Grant Number: Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences; New National Excellence Program of the Ministry for Innovation and Technology from the source of the National Research, Development and Innovation Found [UNKP-21-5-SZTE-555]; European Union [754432]; Polish Ministry of Science and Higher Education; SZTEAOK-KKA [5S 567 (A202)]; Developing Scientific Workshops of Medical-, Health Sciences and Pharmaceutical Training (Hungary) [EFOP 3.6.3-VEKOP-16-201700009] Funding text: This project was supported by the J ' anos Bolyai Research Scholarship of the Hungarian Academy of Sciences; by the UNKP-21-5-SZTE-555 New National Excellence Program of the Ministry for Innovation and Technology from the source of the National Research, Development and Innovation Found; by the European Union's Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie grant agreement, Nr. 754432; by the Polish Ministry of Science and Higher Education; by the SZTE ' AOK-KKA No. 5S 567 (A202) and by the Developing Scientific Workshops of Medical-, Health Sciences and Pharmaceutical Training (grant number: EFOP 3.6.3-VEKOP-16-201700009; Hungary). LA - English DB - MTMT ER - TY - JOUR AU - Szögi, Titanilla AU - Borbély, Emőke AU - Schuster, Ildikó AU - Bozsó, Zsolt AU - Sántha, Miklós AU - Tóth, Erzsébet Melinda AU - Penke, Botond AU - Fülöp, Lívia TI - Examination of Longitudinal Alterations in Alzheimer’s Disease-Related Neurogenesis in an APP/PS1 Transgenic Mouse Model, and the Effects of P33, a Putative Neuroprotective Agent Thereon JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 23 PY - 2022 IS - 18 PG - 17 SN - 1661-6596 DO - 10.3390/ijms231810364 UR - https://m2.mtmt.hu/api/publication/33111245 ID - 33111245 N1 - Funding Agency and Grant Number: National Research, Development and Innovation Office [GINOP-2.3.2-15-2016-00060]; Hungarian Brain Research Program I and II [KTIA_13_NAP-A-III/7, 2017-1.2.1-NKP-2017-00002]; Ministry of Human Capacities, Hungary [20391-3/2018/FEKUSTRAT]; Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund [TKP2021-EGA-32] Funding text: This project was supported by the National Research, Development and Innovation Office (GINOP-2.3.2-15-2016-00060) and by the Hungarian Brain Research Program I and II (Grant No. KTIA_13_NAP-A-III/7, and 2017-1.2.1-NKP-2017-00002). Support by the Ministry of Human Capacities, Hungary (grant 20391-3/2018/FEKUSTRAT) and the Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund (TKP2021-EGA-32) is acknowledged. AB - Neurogenesis plays a crucial role in cognitive processes. During aging and in Alzheimer’s disease (AD), altered neurogenesis and neuroinflammation are evident both in C57BL/6J, APPSwe/PS1dE9 (Tg) mice and humans. AD pathology may slow down upon drug treatment, for example, in a previous study of our group P33, a putative neuroprotective agent was found to exert advantageous effects on the elevated levels of APP, Aβ, and neuroinflammation. In the present study, we aimed to examine longitudinal alterations in neurogenesis, neuroinflammation and AD pathology in a transgenic (Tg) mouse model, and assessed the putative beneficial effects of long-term P33 treatment on AD-specific neurological alterations. Hippocampal cell proliferation and differentiation were significantly reduced between 8 and 12 months of age. Regarding neuroinflammation, significantly elevated astrogliosis and microglial activation were observed in 6- to 7-month-old Tg animals. The amounts of the molecules involved in the amyloidogenic pathway were altered from 4 months of age in Tg animals. P33-treatment led to significantly increased neurogenesis in 9-month-old animals. Our data support the hypothesis that altered neurogenesis may be a consequence of AD pathology. Based on our findings in the transgenic animal model, early pharmacological treatment before the manifestation of AD symptoms might ameliorate neurological decline. LA - English DB - MTMT ER - TY - JOUR AU - Fodor, István AU - Svigruha, Réka AU - Bozsó, Zsolt AU - Tóth, Gábor AU - Tomohiro, Osugi AU - Tatsuya, Yamamoto AU - Honoo, Satake AU - Pirger, Zsolt TI - Functional characterization and related evolutionary implications of invertebrate gonadotropin-releasing hormone/corazonin in a well-established model species JF - SCIENTIFIC REPORTS J2 - SCI REP VL - 11 PY - 2021 IS - 1 PG - 10 SN - 2045-2322 DO - 10.1038/s41598-021-89614-5 UR - https://m2.mtmt.hu/api/publication/31997552 ID - 31997552 N1 - Funding Agency and Grant Number: National Brain Project [2017-1.2.1-NKP-2017-00002] Funding text: This work was supported by National Brain Project (No. 2017-1.2.1-NKP-2017-00002). LA - English DB - MTMT ER - TY - JOUR AU - Ibos, Katalin Eszter AU - Bodnár, Éva AU - Bagosi, Zsolt AU - Bozsó, Zsolt AU - Tóth, Gábor AU - Szabó, Gyula AU - Csabafi, Krisztina TI - Kisspeptin-8 Induces Anxiety-Like Behavior and Hypolocomotion by Activating the HPA Axis and Increasing GABA Release in the Nucleus Accumbens in Rats JF - BIOMEDICINES J2 - BIOMEDICINES VL - 9 PY - 2021 IS - 2 PG - 22 SN - 2227-9059 DO - 10.3390/biomedicines9020112 UR - https://m2.mtmt.hu/api/publication/31829118 ID - 31829118 N1 - Department of Pathophysiology, Faculty of Medicine, University of Szeged, Szeged, H-6720, Hungary Department of Medical Chemistry, Faculty of Medicine, University of Szeged, Szeged, H-6720, Hungary Office of International Affairs, Budapest Campus, McDaniel College, Budapest, H-1071, Hungary Export Date: 8 February 2021 Correspondence Address: Ibos, K.E.; Department of Pathophysiology, Hungary; email: ibos.katalin.eszter@med.u-szeged.hu Funding details: European Commission, EC, EFOP-3.6.2-16-2017-00006 Funding details: Magyarország Kormánya Funding text 1: Funding: This research was funded by the Hungarian Government and the European Union through the EFOP-3.6.2-16-2017-00006 grant. Department of Pathophysiology, Faculty of Medicine, University of Szeged, Szeged, H-6720, Hungary Department of Medical Chemistry, Faculty of Medicine, University of Szeged, Szeged, H-6720, Hungary Office of International Affairs, Budapest Campus, McDaniel College, Budapest, H-1071, Hungary Export Date: 9 February 2021 Correspondence Address: Ibos, K.E.; Department of Pathophysiology, Hungary; email: ibos.katalin.eszter@med.u-szeged.hu Funding details: European Commission, EC, EFOP-3.6.2-16-2017-00006 Funding details: Magyarország Kormánya Funding text 1: Funding: This research was funded by the Hungarian Government and the European Union through the EFOP-3.6.2-16-2017-00006 grant. LA - English DB - MTMT ER - TY - JOUR AU - Balázs, Evelin AU - Oláh, Zita AU - Gálik, Bence AU - Bozsó, Zsolt AU - Kálmán, János AU - Datki, Zsolt László TI - Neurodegeneration-related beta-amyloid as autocatabolism-attenuator in a micro-in vivo system JF - IBRO REPORTS J2 - IBRO REP VL - 9 PY - 2020 SP - 319 EP - 323 PG - 5 SN - 2451-8301 DO - 10.1016/j.ibror.2020.10.002 UR - https://m2.mtmt.hu/api/publication/31639846 ID - 31639846 LA - English DB - MTMT ER - TY - CHAP AU - Tóth, Gábor AU - Bogár, Ferenc AU - Bozsó, Zsolt AU - Szolomájer, János AU - Kele, Zoltán AU - Csóti, Ágota AU - Szántó, Gábor Tibor AU - Panyi, György ED - Rakonczay, Zoltán ED - Kiss, Lóránd TI - Design and synthesis of selective ion channel blocker peptide toxin analogues T2 - Proceedings of the EFOP-3.6.2-16-2017-00006 (LIVE LONGER) project PB - University of Szeged CY - Szeged SN - 9789633067642 PY - 2020 SP - 75 UR - https://m2.mtmt.hu/api/publication/31642870 ID - 31642870 LA - English DB - MTMT ER - TY - CHAP AU - Tóth, Gábor AU - Bozsó, Zsolt AU - Szolomájer, János AU - Kele, Zoltán AU - Zoltán, Pethő AU - János, Almássy AU - Zoltán, Varga ED - Rakonczay, Zoltán ED - Kiss, Lóránd TI - Synthesis of ryanodine receptor selective charybdotoxin analogues T2 - Proceedings of the EFOP-3.6.2-16-2017-00006 (LIVE LONGER) project PB - University of Szeged CY - Szeged SN - 9789633067642 PY - 2020 SP - 74 UR - https://m2.mtmt.hu/api/publication/31642862 ID - 31642862 LA - English DB - MTMT ER -