@article{MTMT:34395398, title = {Role of the kisspeptin-KISS1R axis in the pathogenesis of chronic kidney disease and uremic cardiomyopathy}, url = {https://m2.mtmt.hu/api/publication/34395398}, author = {Dinh, Hoa and Kovács, Zsuzsanna and Kis, Merse and Kupecz, Klaudia and Sejben, Anita and Szűcs, Gergő and Márványkövi, Fanni and Siska, Andrea and Freiwan, Marah and Pósa, Szonja Polett and Galla, Zsolt and Ibos, Katalin Eszter and Bodnár, Éva and Lauber, Gülsüm Yilmaz and Goncalves, Ana Isabel Antunes and Acar, Eylem and Kriston, András and Kovács, Ferenc and Horváth, Péter and Bozsó, Zsolt and Tóth, Gábor and Földesi, Imre and Monostori, Péter and Cserni, Gábor and Podesser, Bruno K. and Lehoczki, Andrea and Pokreisz, Peter and Kiss, Attila and Dux, László and Csabafi, Krisztina and Sárközy, Márta}, doi = {10.1007/s11357-023-01017-8}, journal-iso = {GEROSCIENCE}, journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)}, volume = {46}, unique-id = {34395398}, issn = {2509-2715}, abstract = {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.}, year = {2024}, eissn = {2509-2723}, pages = {2463-2488}, orcid-numbers = {Kovács, Zsuzsanna/0000-0002-4197-4579; Sejben, Anita/0000-0002-9434-2989; Szűcs, Gergő/0000-0003-1874-2718; Márványkövi, Fanni/0000-0002-5114-1319; Pósa, Szonja Polett/0000-0002-7535-9689; Galla, Zsolt/0000-0002-9166-1212; Ibos, Katalin Eszter/0000-0001-5243-9945; Goncalves, Ana Isabel Antunes/0009-0009-3428-3321; Acar, Eylem/0000-0002-0599-6893; Kriston, András/0000-0001-8500-4315; Bozsó, Zsolt/0000-0002-5713-3096; Tóth, Gábor/0000-0002-3604-4385; Földesi, Imre/0000-0002-3329-8136; Monostori, Péter/0000-0003-3591-6054; Cserni, Gábor/0000-0003-1344-7744; Podesser, Bruno K./0000-0002-4641-7202; Lehoczki, Andrea/0000-0002-4285-7518; Pokreisz, Peter/0000-0003-2810-9000; Kiss, Attila/0000-0003-4652-1998; Dux, László/0000-0002-1270-1678; Csabafi, Krisztina/0000-0002-2008-7604; Sárközy, Márta/0000-0002-5929-2146} } @article{MTMT:34050718, title = {The Nuclear Localization Signal of NF-κB p50 Enters the Cells via Syndecan-Mediated Endocytosis and Inhibits NF-κB Activity}, url = {https://m2.mtmt.hu/api/publication/34050718}, author = {Letoha, Annamária and Hudák, Anett and Bozsó, Zsolt and Vizler, Csaba and Veres, Gábor and Szilák, László and Letoha, Tamás}, doi = {10.1007/s10989-023-10548-9}, journal-iso = {INT J PEPT RES THER}, journal = {INTERNATIONAL JOURNAL OF PEPTIDE RESEARCH AND THERAPEUTICS}, volume = {29}, unique-id = {34050718}, issn = {1573-3149}, abstract = {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.}, year = {2023}, eissn = {1573-3904} } @article{MTMT:32753550, title = {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}, url = {https://m2.mtmt.hu/api/publication/32753550}, author = {Borbély, Emőke and Varga, Viktória and Szögi, Titanilla and Schuster, Ildikó and Bozsó, Zsolt and Penke, Botond and Fülöp, Lívia}, doi = {10.3390/ijms23052514}, journal-iso = {INT J MOL SCI}, journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES}, volume = {23}, unique-id = {32753550}, issn = {1661-6596}, year = {2022}, eissn = {1422-0067}, orcid-numbers = {Szögi, Titanilla/0000-0002-9854-7340; Schuster, Ildikó/0000-0001-9997-5729; Bozsó, Zsolt/0000-0002-5713-3096; Penke, Botond/0000-0003-0938-0567; Fülöp, Lívia/0000-0002-8010-0129} } @article{MTMT:32591465, title = {The interacting rotifer-biopolymers are anti- and disaggregating agents for human-type beta-amyloid in vitro}, url = {https://m2.mtmt.hu/api/publication/32591465}, author = {Datki, Zsolt László and Balázs, Evelin and Gálik, Bence and Sinka, Rita and Zeitler, Lavínia and Bozsó, Zsolt and Kálmán, János and Hortobágyi, Tibor and Oláh, Zita}, doi = {10.1016/j.ijbiomac.2021.12.184}, journal-iso = {INT J BIOL MACROMOL}, journal = {INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES}, volume = {201}, unique-id = {32591465}, issn = {0141-8130}, year = {2022}, eissn = {1879-0003}, pages = {262-269}, orcid-numbers = {Datki, Zsolt László/0000-0002-2537-4741; Sinka, Rita/0000-0003-4040-4184; Bozsó, Zsolt/0000-0002-5713-3096; Kálmán, János/0000-0001-5319-5639; Hortobágyi, Tibor/0000-0001-5732-7942; Oláh, Zita/0000-0002-6372-532X} } @article{MTMT:33111245, title = {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}, url = {https://m2.mtmt.hu/api/publication/33111245}, author = {Szögi, Titanilla and Borbély, Emőke and Schuster, Ildikó and Bozsó, Zsolt and Sántha, Miklós and Tóth, Erzsébet Melinda and Penke, Botond and Fülöp, Lívia}, doi = {10.3390/ijms231810364}, journal-iso = {INT J MOL SCI}, journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES}, volume = {23}, unique-id = {33111245}, issn = {1661-6596}, abstract = {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.}, year = {2022}, eissn = {1422-0067}, orcid-numbers = {Szögi, Titanilla/0000-0002-9854-7340; Schuster, Ildikó/0000-0001-9997-5729; Bozsó, Zsolt/0000-0002-5713-3096; Penke, Botond/0000-0003-0938-0567; Fülöp, Lívia/0000-0002-8010-0129} } @article{MTMT:31997552, title = {Functional characterization and related evolutionary implications of invertebrate gonadotropin-releasing hormone/corazonin in a well-established model species}, url = {https://m2.mtmt.hu/api/publication/31997552}, author = {Fodor, István and Svigruha, Réka and Bozsó, Zsolt and Tóth, Gábor and Tomohiro, Osugi and Tatsuya, Yamamoto and Honoo, Satake and Pirger, Zsolt}, doi = {10.1038/s41598-021-89614-5}, journal-iso = {SCI REP}, journal = {SCIENTIFIC REPORTS}, volume = {11}, unique-id = {31997552}, issn = {2045-2322}, year = {2021}, eissn = {2045-2322}, orcid-numbers = {Pirger, Zsolt/0000-0001-9039-6966} } @article{MTMT:31829118, title = {Kisspeptin-8 Induces Anxiety-Like Behavior and Hypolocomotion by Activating the HPA Axis and Increasing GABA Release in the Nucleus Accumbens in Rats}, url = {https://m2.mtmt.hu/api/publication/31829118}, author = {Ibos, Katalin Eszter and Bodnár, Éva and Bagosi, Zsolt and Bozsó, Zsolt and Tóth, Gábor and Szabó, Gyula and Csabafi, Krisztina}, doi = {10.3390/biomedicines9020112}, journal-iso = {BIOMEDICINES}, journal = {BIOMEDICINES}, volume = {9}, unique-id = {31829118}, year = {2021}, eissn = {2227-9059}, orcid-numbers = {Ibos, Katalin Eszter/0000-0001-5243-9945; Bozsó, Zsolt/0000-0002-5713-3096; Tóth, Gábor/0000-0002-3604-4385; Szabó, Gyula/0000-0002-3409-5357; Csabafi, Krisztina/0000-0002-2008-7604} } @article{MTMT:31639846, title = {Neurodegeneration-related beta-amyloid as autocatabolism-attenuator in a micro-in vivo system}, url = {https://m2.mtmt.hu/api/publication/31639846}, author = {Balázs, Evelin and Oláh, Zita and Gálik, Bence and Bozsó, Zsolt and Kálmán, János and Datki, Zsolt László}, doi = {10.1016/j.ibror.2020.10.002}, journal-iso = {IBRO REP}, journal = {IBRO REPORTS}, volume = {9}, unique-id = {31639846}, year = {2020}, eissn = {2451-8301}, pages = {319-323}, orcid-numbers = {Oláh, Zita/0000-0002-6372-532X; Bozsó, Zsolt/0000-0002-5713-3096; Kálmán, János/0000-0001-5319-5639; Datki, Zsolt László/0000-0002-2537-4741} } @{MTMT:31642870, title = {Design and synthesis of selective ion channel blocker peptide toxin analogues}, url = {https://m2.mtmt.hu/api/publication/31642870}, author = {Tóth, Gábor and Bogár, Ferenc and Bozsó, Zsolt and Szolomájer, János and Kele, Zoltán and Csóti, Ágota and Szántó, Gábor Tibor and Panyi, György}, booktitle = {Proceedings of the EFOP-3.6.2-16-2017-00006 (LIVE LONGER) project}, unique-id = {31642870}, year = {2020}, pages = {75}, orcid-numbers = {Panyi, György/0000-0001-6227-3301} } @{MTMT:31642862, title = {Synthesis of ryanodine receptor selective charybdotoxin analogues}, url = {https://m2.mtmt.hu/api/publication/31642862}, author = {Tóth, Gábor and Bozsó, Zsolt and Szolomájer, János and Kele, Zoltán and Zoltán, Pethő and János, Almássy and Zoltán, Varga}, booktitle = {Proceedings of the EFOP-3.6.2-16-2017-00006 (LIVE LONGER) project}, unique-id = {31642862}, year = {2020}, pages = {74} }