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 - Ibos, Katalin Eszter AU - Bodnár, Éva AU - Dinh, Hoa AU - Kis, Merse AU - Márványkövi, Fanni AU - Kovács, Zsuzsanna AU - Siska, Andrea AU - Földesi, Imre AU - Galla, Zsolt AU - Monostori, Péter AU - Szatmári, István AU - Simon, Péter AU - Sárközy, Márta AU - Csabafi, Krisztina TI - Chronic kidney disease may evoke anxiety by altering CRH expression in the amygdala and tryptophan metabolism in rats JF - PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY J2 - PFLUG ARCH EUR J PHY VL - 476 PY - 2024 IS - 2 SP - 179 EP - 196 PG - 18 SN - 0031-6768 DO - 10.1007/s00424-023-02884-y UR - https://m2.mtmt.hu/api/publication/34394136 ID - 34394136 AB - Chronic kidney disease (CKD) is associated with anxiety; however, its exact mechanism is not well understood. Therefore, the aim of the present study was to assess the effect of moderate CKD on anxiety in rats. 5/6 nephrectomy was performed in male Wistar rats. 7 weeks after, anxiety-like behavior was assessed by elevated plus maze (EPM), open field (OF), and marble burying (MB) tests. At weeks 8 and 9, urinalysis was performed, and blood and amygdala samples were collected, respectively. In the amygdala, the gene expression of Avp and the gene and protein expression of Crh , Crhr1 , and Crhr2 were analyzed. Furthermore, the plasma concentration of corticosterone, uremic toxins, and tryptophan metabolites was measured by UHPLC-MS/MS. Laboratory tests confirmed the development of CKD. In the CKD group, the closed arm time increased; the central time and the total number of entries decreased in the EPM. There was a reduction in rearing, central distance and time in the OF, and fewer interactions with marbles were detected during MB. CKD evoked an upregulation of gene expression of Crh , Crhr1 , and Crhr2 , but not Avp , in the amygdala. However, there was no alteration in protein expression. In the CKD group, plasma concentrations of p-cresyl-sulfate, indoxyl-sulfate, kynurenine, kynurenic acid, 3-hydroxykynurenine, anthranilic acid, xanthurenic acid, 5-hydroxyindoleacetic acid, picolinic acid, and quinolinic acid increased. However, the levels of tryptophan, tryptamine, 5-hydroxytryptophan, serotonin, and tyrosine decreased. In conclusion, moderate CKD evoked anxiety-like behavior that might be mediated by the accumulation of uremic toxins and metabolites of the kynurenine pathway, but the contribution of the amygdalar CRH system to the development of anxiety seems to be negligible at this stage. LA - English DB - MTMT ER - TY - BOOK ED - Tolnai, József ED - Peták, Ferenc ED - Fodor, Gergely ED - Rakonczay, Zoltán TI - 2023. évi Orvos- és Egészségtudományi TDK Konferencia PB - Szegedi Tudományegyetem CY - Szeged PY - 2023 SP - 301 SN - 9789633069592 UR - https://m2.mtmt.hu/api/publication/34446677 ID - 34446677 LA - English DB - MTMT ER - TY - JOUR AU - Csabafi, Krisztina AU - Ibos, Katalin Eszter AU - Bodnár, Éva AU - Filkor, Kata AU - Szakács, Júlia AU - Bagosi, Zsolt TI - A Brain Region-Dependent Alteration in the Expression of Vasopressin, Corticotropin-Releasing Factor, and Their Receptors Might Be in the Background of Kisspeptin-13-Induced Hypothalamic-Pituitary-Adrenal Axis Activation and Anxiety in Rats JF - BIOMEDICINES J2 - BIOMEDICINES VL - 11 PY - 2023 IS - 9 PG - 20 SN - 2227-9059 DO - 10.3390/biomedicines11092446 UR - https://m2.mtmt.hu/api/publication/34193757 ID - 34193757 N1 - Export Date: 24 October 2023 Correspondence Address: Csabafi, K.; Department of Pathophysiology, P.O. Box 427, Hungary; email: csabafi.krisztina@med.u-szeged.hu Funding text 1: This research was funded by SZAOK-KKA-SZGYA: 2023.02.01.–2025.01.30. AB - Previously, we reported that intracerebroventricularly administered kisspeptin-13 (KP-13) induces anxiety-like behavior and activates the hypothalamic-pituitary-adrenal (HPA) axis in rats. In the present study, we aimed to shed light on the mediation of KP-13′s stress-evoking actions. The relative gene expressions of the corticotropin-releasing factor (Crf, Crfr1, and Crfr2) and arginine vasopressin (Avp, Avpr1a, and Avpr1b) systems were measured in the amygdala and hippocampus of male Wistar rats after icv KP-13 treatment. CRF and AVP protein content were also determined. A different set of animals received CRF or V1 receptor antagonist pretreatment before the KP-13 challenge, after which either an open-field test or plasma corticosterone levels measurement was performed. In the amygdala, KP-13 induced an upregulation of Avp and Avpr1b expression, and a downregulation of Crf. In the hippocampus, the mRNA level of Crf increased and the level of Avpr1a decreased. A significant rise in AVP protein content was also detected in the amygdala. KP-13 also evoked anxiety-like behavior in the open field test, which the V1 receptor blocker antagonized. Both CRF and V1 receptor blockers reduced the KP-13-evoked rise in the plasma corticosterone level. This suggests that KP-13 alters the AVP and CRF signaling and that might be responsible for its effect on the HPA axis and anxiety-like behavior. LA - English DB - MTMT ER - TY - JOUR AU - Ayman, Jázmin AU - Palotai, M. AU - Dochnal, Roberta AU - Bagosi, Zsolt TI - Ghrelin Amplifies the Nicotine-Induced Release of Dopamine in the Bed Nucleus of Stria Terminalis (BNST) JF - BIOMEDICINES J2 - BIOMEDICINES VL - 11 PY - 2023 IS - 9 PG - 13 SN - 2227-9059 DO - 10.3390/biomedicines11092456 UR - https://m2.mtmt.hu/api/publication/34189729 ID - 34189729 LA - English DB - MTMT ER - TY - JOUR AU - Orján, Erik Márk AU - Kormányos, Eszter Sára AU - Fűr, Gabriella AU - Dombi, Ágnes AU - Bálint, Emese Réka AU - Balla, Zsolt AU - Balog, Beáta Adél AU - Dágó, Ágnes AU - Totonji, Ahmad AU - Bátai, István Zoárd AU - Jurányi, Eszter Petra AU - Ditrói, Tamás AU - Al-omari, Ammar AU - Pozsgai, Gábor AU - Kormos, Viktória AU - Nagy, Péter AU - Pintér, Erika AU - Rakonczay, Zoltán AU - Kiss, Lóránd TI - The anti-inflammatory effect of dimethyl trisulfide in experimental acute pancreatitis JF - SCIENTIFIC REPORTS J2 - SCI REP VL - 13 PY - 2023 IS - 1 PG - 19 SN - 2045-2322 DO - 10.1038/s41598-023-43692-9 UR - https://m2.mtmt.hu/api/publication/34183455 ID - 34183455 N1 - * Megosztott szerzőség AB - Various organosulfur compounds, such as dimethyl trisulfide (DMTS), display anti-inflammatory properties. We aimed to examine the effects of DMTS on acute pancreatitis (AP) and its mechanism of action in both in vivo and in vitro studies. AP was induced in FVB/n mice or Wistar rats by caerulein, ethanol-palmitoleic acid, or L-ornithine-HCl. DMTS treatments were administered subcutaneously. AP severity was assessed by pancreatic histological scoring, pancreatic water content, and myeloperoxidase activity measurements. The behaviour of animals was followed. Pancreatic heat shock protein 72 (HSP72) expression, sulfide, and protein persulfidation were measured. In vitro acinar viability, intracellular Ca 2+ concentration, and reactive oxygen species production were determined. DMTS dose-dependently decreased the severity of AP. It declined the pancreatic infiltration of leukocytes and cellular damage in mice. DMTS upregulated the HSP72 expression during AP and elevated serum sulfide and low molecular weight persulfide levels. DMTS exhibited cytoprotection against hydrogen peroxide and AP-inducing agents. It has antioxidant properties and modulates physiological but not pathophysiological Ca 2+ signalling. Generally, DMTS ameliorated AP severity and protected pancreatic acinar cells. Our findings indicate that DMTS is a sulfur donor with anti-inflammatory and antioxidant effects, and organosulfur compounds require further investigation into this potentially lethal disease. LA - English DB - MTMT ER - TY - JOUR AU - Simon, Balázs AU - Thury, Attila Ágoston AU - Török, László AU - Földesi, Imre AU - Csabafi, Krisztina AU - Bagosi, Zsolt TI - The effects of alcohol on anxiety-like, depression-like, and social behavior immediately and a day after binge drinking JF - ALCOHOL J2 - ALCOHOL VL - 112 PY - 2023 SP - 17 EP - 24 PG - 8 SN - 0741-8329 DO - 10.1016/j.alcohol.2023.05.004 UR - https://m2.mtmt.hu/api/publication/34182063 ID - 34182063 N1 - Department of Pathophysiology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary Department of Traumatology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary Institute of Laboratory Medicine, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary Export Date: 11 October 2023 CODEN: ALCOE Correspondence Address: Simon, B.; Department of Pathophysiology, Semmelweis str. 1 Szeged, Hungary; email: dr.simon.balazs@live.com LA - English DB - MTMT ER - TY - JOUR AU - Kemenesi-Gedei, Péter Bátor AU - Csabafi, Krisztina AU - Karcsúné Kis, Gyöngyi TI - Inflammatory Orofacial Pain Activates Peptidergic Neurons and Upregulates the Oxytocin Receptor Expression in Trigeminal Ganglion JF - BIOMEDICINES J2 - BIOMEDICINES VL - 11 PY - 2023 IS - 9 PG - 12 SN - 2227-9059 DO - 10.3390/biomedicines11092419 UR - https://m2.mtmt.hu/api/publication/34124825 ID - 34124825 AB - The majority of orofacial pain is caused by musculoskeletal and neuropathological diseases related to inflammatory processes that lead even to transcriptional alterations in the trigeminal ganglion (TG) neurons. The hypothalamic nonapeptide oxytocin has been reported to modulate nociception via binding and activating its receptor in primary sensory neurons. The purpose of this study was to analyze the gene expression of the oxytocin receptor (OTR), c-Fos, an indicator of neuronal activity, and α-calcitonin gene-related peptide (αCGRP), a characteristic neurotransmitter of the peptidergic trigeminal primary afferents in an animal model of inflammation-induced orofacial pain. Carrageenan was unilaterally injected into the vibrissal pads of male and female adult Wistar rats. RT-qPCR was performed to analyze the levels of mRNA expression in TGs 24 h after injection. The gene expression analysis revealed higher fold changes regarding the c-Fos (mean ± S.E: ♀: 3.9 ± 0.19; ♂: 3.55 ± 0.18) and αCGRP (♀: 2.84 ± 0.13; ♂: 3.39 ± 0.47) expression levels of mRNA, and a moderate rise in the expression of the OTR mRNA (♀: 1.52 ± 0.07; ♂: 1.49 ± 0.07) was observed in comparison to both vehicle(saline)-treated and untreated controls. Our results furnish evidence for inflammation-induced activation of peptidergic neurons, and it is suggested that oxytocin modulates inflammation-induced nociception by enhancing their signaling capacity due to its elevated expression in the sensory ganglion cells, thus providing new therapies for orofacial pain relief that target the OTRs. LA - English DB - MTMT ER - TY - JOUR AU - Dinh, Hoa AU - Kovács, Zsuzsanna AU - Márványkövi, Fanni AU - Kis, Merse AU - Kupecz, Klaudia AU - Szűcs, Gergő AU - Freiwan, Marah AU - Lauber, Gülsüm Yilmaz AU - Acar, Eylem AU - Siska, Andrea AU - Ibos, Katalin Eszter AU - Bodnár, Éva AU - Kriston, András AU - Kovács, Ferenc AU - Horváth, Péter AU - Földesi, Imre AU - Cserni, Gábor AU - Podesser, Bruno K. AU - Pokreisz, Peter AU - Kiss, Attila AU - Dux, László AU - Csabafi, Krisztina AU - Sárközy, Márta TI - The kisspeptin-1 receptor antagonist peptide-234 aggravates uremic cardiomyopathy in a rat model JF - SCIENTIFIC REPORTS J2 - SCI REP VL - 13 PY - 2023 IS - 1 PG - 16 SN - 2045-2322 DO - 10.1038/s41598-023-41037-0 UR - https://m2.mtmt.hu/api/publication/34123594 ID - 34123594 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 Ludwig Boltzmann Institute for Cardiovascular Research at Center for Biomedical Research and Translational Surgery, Medical University of Vienna, Vienna, A1090, Austria Department of Laboratory Medicine, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary Department of Pathophysiology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary 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 Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, 6720, Hungary Export Date: 7 September 2023 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: sarkozy.marta@med.u-szeged.hu Funding details: BO/00532/23/5, UNKP-19-3-SZTE-160, UNKP-20-5-SZTE-166 Funding details: TSZ:34232-3/2016/INTFIN Funding details: 6177 Funding details: Magyar Tudományos Akadémia, MTA Funding details: Nemzeti Kutatási Fejlesztési és Innovációs Hivatal, NKFIH, EFOP-3.6.2-16-2017-00006, GINOP-2.3.2-15-2016-00040 Funding details: Tempus Közalapítvány, TPF Funding details: Szegedi Tudományegyetem, SZTE Funding text 1: Open access funding provided by University of Szeged. This research was funded by the projects NKFIH FK129094 (to M.S., funder: National Research, Development and Innovation Office), GINOP-2.3.2-15-2016-00040 (to L.D., funder: National Research, Development and Innovation Office), EFOP-3.6.2-16-2017-00006 (to K.C., funder: National Research, Development and Innovation Office), Stipendium Hungaricum Program (to M.S. and L.D., funder: Tempus Public Foundation), and Ludwig Boltzmann Institute for Cardiovascular Research, Vienna, Austria. D.H. and M.F. were supported by the Stipendium Hungaricum Scholarship (funder: Tempus Public Foundation). H. D. was supported by the Albert Szent-Györgyi Scholarship for Ph.D. students (funder: University of Szeged, Albert Szent-Györgyi Medical School, Szeged, Hungary) and Bach Mai Hospital, Hanoi, Vietnam. M.S. and Z.Z.A.K. were supported by the New National Excellence Program of the Ministry of Human Capacities, Hungary (UNKP-20-5-SZTE-166 and UNKP-19-3-SZTE-160). M.S. was supported by the János Bolyai Research Scholarship (BO/00532/23/5) of the Hungarian Academy of Sciences. Z.Z.A.K. was supported by the EFOP 3.6.3-VEKOP-16-2017-00009 (funder: National Research, Development and Innovation Office). A.K. was supported by Theodor Körner Founds, Austria. F.M. was supported by the Szeged Scientists Academy Program (TSZ:34232-3/2016/INTFIN, Hungary). The publication was supported by the University of Szeged Open Access Found (6177). AB - Uremic cardiomyopathy is characterized by diastolic dysfunction, left ventricular hypertrophy (LVH), and fibrosis. Dysregulation of the kisspeptin receptor (KISS1R)-mediated pathways are associated with the development of fibrosis in cancerous diseases. Here, we investigated the effects of the KISS1R antagonist peptide-234 (P234) on the development of uremic cardiomyopathy. Male Wistar rats (300–350 g) were randomized into four groups: (i) Sham, (ii) chronic kidney disease (CKD) induced by 5/6 nephrectomy, (iii) CKD treated with a lower dose of P234 ( ip. 13 µg/day), (iv) CKD treated with a higher dose of P234 ( ip. 26 µg/day). Treatments were administered daily from week 3 for 10 days. At week 13, the P234 administration did not influence the creatinine clearance and urinary protein excretion. However, the higher dose of P234 led to reduced anterior and posterior wall thicknesses, more severe interstitial fibrosis, and overexpression of genes associated with left ventricular remodeling ( Ctgf, Tgfb, Col3a1, Mmp9 ), stretch ( Nppa ), and apoptosis ( Bax, Bcl2, Casp7 ) compared to the CKD group. In contrast, no significant differences were found in the expressions of apoptosis-associated proteins between the groups. Our results suggest that the higher dose of P234 hastens the development and pathophysiology of uremic cardiomyopathy by activating the fibrotic TGF-β-mediated pathways. LA - English DB - MTMT ER - TY - THES AU - Kormányos, Eszter Sára TI - Improving the outcome of experimental acute pancreatitis: the effects of kynurenic acid, SZR-72 and analgesia [A kísérletes akut hasnyálmirigy-gyulladás kimenetelének javítása: a kinurénsav, az SZR-72 és a fájdalomcsillapítás hatása] PB - Szegedi Tudományegyetem PY - 2023 SP - 54 DO - 10.14232/phd.11543 UR - https://m2.mtmt.hu/api/publication/34112876 ID - 34112876 LA - English DB - MTMT ER -