TY - JOUR AU - Ébert, Attila AU - Gál, Eleonóra AU - Tóth, Emese AU - Szögi, Titanilla AU - Hegyi, Péter AU - Venglovecz, Viktória TI - Role of CFTR in diabetes‐induced pancreatic ductal fluid and HCO 3 − secretion JF - JOURNAL OF PHYSIOLOGY-LONDON J2 - J PHYSIOL-LONDON VL - 602 PY - 2024 IS - 6 SP - 1065 EP - 1083 PG - 19 SN - 0022-3751 DO - 10.1113/JP285702 UR - https://m2.mtmt.hu/api/publication/34677129 ID - 34677129 N1 - Funding Agency and Grant Number: CF-Trust CFRD-SRC [SRC 007]; National Research, Development and Innovation Office [SNN134497]; New National Excellence Program Of The Ministry Of Human Capacities [UNKP-18-4] Funding text: We are grateful for support for this study provided by the CF-Trust CFRD-SRC Grant (No.: SRC 007) and the National Research, Development and Innovation Office (SNN134497) and New National Excellence Program Of The Ministry Of Human Capacities (UNKP-18-4 to VV). LA - English DB - MTMT ER - TY - CONF AU - Apróné Török, Ibolya AU - Seprényi, György AU - Pór, Erzsébet AU - Borbély, Emőke AU - Szögi, Titanilla AU - Dobó, Endre TI - Post-diaminoenzidine treatments for double stainings : extension of sulfide-silver-gold internsification for light and fluorescent microscopy T2 - Magyar Anatómus Társaság 2022. évi konferenciája PB - Szegedi Tudományegyetem Általános Orvostudományi Kar, Anatómiai, Szövet-és Fejlődéstani Intézet C1 - Szeged PY - 2022 SP - 60 EP - 60 PG - 1 UR - https://m2.mtmt.hu/api/publication/33570390 ID - 33570390 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 - 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 - Dukay, Brigitta AU - Walter, Fruzsina AU - Vigh, Judit Piroska AU - Barabási, Beáta AU - Hajdu, Petra AU - Balassa, Tamás AU - Migh, Ede AU - Kincses, András AU - Hoyk, Zsófia AU - Szögi, Titanilla AU - Borbély, Emőke AU - Csoboz, Bálint AU - Horváth, Péter AU - Fülöp, Lívia AU - Penke, Botond AU - Vigh, László AU - Deli, Mária Anna AU - Sántha, Miklós AU - Tóth, Erzsébet Melinda TI - Neuroinflammatory processes are augmented in mice overexpressing human heat-shock protein B1 following ethanol-induced brain injury JF - JOURNAL OF NEUROINFLAMMATION J2 - J NEUROINFLAMM VL - 18 PY - 2021 IS - 1 PG - 24 SN - 1742-2094 DO - 10.1186/s12974-020-02070-2 UR - https://m2.mtmt.hu/api/publication/31807147 ID - 31807147 N1 - Miklós Sántha and Melinda E. Tóth are shared last authors. LA - English DB - MTMT ER - TY - JOUR AU - Apróné Török, Ibolya AU - Seprényi, György AU - Pór, Erzsébet AU - Borbély, Emőke AU - Szögi, Titanilla AU - Dobó, Endre TI - Post-diaminobenzidine Treatments for Double Stainings. Extension of Sulfide-Silver-Gold Intensification for Light and Fluorescent Microscopy TS - Extension of Sulfide-Silver-Gold Intensification for Light and Fluorescent Microscopy JF - JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY J2 - J HISTOCHEM CYTOCHEM VL - 68 PY - 2020 IS - 8 SP - 571 EP - 582 PG - 12 SN - 0022-1554 DO - 10.1369/0022155420942213 UR - https://m2.mtmt.hu/api/publication/31439812 ID - 31439812 N1 - Department of Anatomy, Faculty of Medicine, University of Szeged, Szeged, Hungary Department of Medical Chemistry, Faculty of Medicine, University of Szeged, Szeged, Hungary Export Date: 31 March 2021 CODEN: JHCYA Correspondence Address: Dobó, E.; Department of Anatomy, Hungary; email: dobo.endre@med.u-szeged.hu Chemicals/CAS: diaminobenzidine, 7411-49-6, 91-95-2; peroxidase, 9003-99-0; gold, 7440-57-5; 3,3'-Diaminobenzidine; Gold; Silver Compounds; silver sulfide Funding text 1: The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This study was supported by the Department of Anatomy, Faculty of Medicine, University of Szeged funds. Department of Anatomy, Faculty of Medicine, University of Szeged, Szeged, Hungary Department of Medical Chemistry, Faculty of Medicine, University of Szeged, Szeged, Hungary Export Date: 14 April 2021 CODEN: JHCYA Correspondence Address: Dobó, E.; Department of Anatomy, Hungary; email: dobo.endre@med.u-szeged.hu Chemicals/CAS: diaminobenzidine, 7411-49-6, 91-95-2; peroxidase, 9003-99-0; gold, 7440-57-5; 3,3'-Diaminobenzidine; Gold; Silver Compounds; silver sulfide Funding text 1: The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This study was supported by the Department of Anatomy, Faculty of Medicine, University of Szeged funds. Department of Anatomy, Faculty of Medicine, University of Szeged, Szeged, Hungary Department of Medical Chemistry, Faculty of Medicine, University of Szeged, Szeged, Hungary Export Date: 20 April 2021 CODEN: JHCYA Correspondence Address: Dobó, E.; Department of Anatomy, Hungary; email: dobo.endre@med.u-szeged.hu Chemicals/CAS: diaminobenzidine, 7411-49-6, 91-95-2; peroxidase, 9003-99-0; gold, 7440-57-5; 3,3'-Diaminobenzidine; Gold; Silver Compounds; silver sulfide Funding text 1: The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This study was supported by the Department of Anatomy, Faculty of Medicine, University of Szeged funds. Department of Anatomy, Faculty of Medicine, University of Szeged, Szeged, Hungary Department of Medical Chemistry, Faculty of Medicine, University of Szeged, Szeged, Hungary Export Date: 23 April 2021 CODEN: JHCYA Correspondence Address: Dobó, E.; Department of Anatomy, Hungary; email: dobo.endre@med.u-szeged.hu Chemicals/CAS: diaminobenzidine, 7411-49-6, 91-95-2; peroxidase, 9003-99-0; gold, 7440-57-5; 3,3'-Diaminobenzidine; Gold; Silver Compounds; silver sulfide Funding text 1: The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This study was supported by the Department of Anatomy, Faculty of Medicine, University of Szeged funds. AB - Double staining protocols using the most popular immunoperoxidase techniques may raise difficulties. The two ordinary detection systems may cross-talk, when the primary antibodies are derived from phylogenetically closely related animals. A color shift of the 3,3 '-diaminobenzidine (DAB) polymer may occur during the second development, resulting in poor distinction between the two kinds of deposits. A post-DAB technique, sulfide-silver-gold intensification, was fine tuned to eliminate these difficulties, which may be especially suitable for colocalization of cell nuclei and perikarya of the same cells. The revised method was probed in combination with a subsequent other immunoperoxidase step or fluorochrome-tagged reagents. The nuclear antigens (BrdU, c-Fos, and Prox-1) were first visualized with DAB polymer, which were then treated with SSGI, turning the deposit black. Thereafter, cytoplasmic antigens (doublecortin, neuronal nuclei, and calbindin) were detected with either another immunoperoxidase using DAB again or immunofluorescence labeling. In both approaches, the immunopositive nuclei and cytoplasmic sites could be easily distinguished even at low magnifications. Different shielding or eluting posttreatments were compared for consecutive acetylcholinesterase histochemistry terminated with DAB development and immunohistochemistry in the same sections. In conclusion, we recommend post-DAB treatments that abolish interactions between detection systems and allow clear distinction between the two signals under various conditions: LA - English DB - MTMT ER - TY - JOUR AU - Szögi, Titanilla AU - Schuster, Ildikó AU - Borbély, Emőke AU - Gyebrovszki, Andrea AU - Bozsó, Zsolt AU - Gera, Janos AU - Rajkó, Róbert AU - Sántha, Miklós AU - Penke, Botond AU - Fülöp, Lívia TI - Effects of the Pentapeptide P33 on Memory and Synaptic Plasticity in APP/PS1 Transgenic Mice: A Novel Mechanism Presenting the Protein Fe65 as a Target JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 20 PY - 2019 IS - 12 PG - 20 SN - 1661-6596 DO - 10.3390/ijms20123050 UR - https://m2.mtmt.hu/api/publication/30744451 ID - 30744451 AB - Regulated intramembrane proteolysis (RIP) of the amyloid precursor protein (APP) leads to the formation of fragments, among which the intracellular domain of APP (AICD) was also identified to be a causative of early pathological events. AICD-counteracting proteins, such as Fe65, may serve as alternative therapeutic targets of Alzheimer's disease (AD). The detection of elevated levels of Fe65 in the brains of both human patients and APP transgenic mice may further strengthen the hypothesis that influencing the interaction between Fe65 and APP may have a beneficial effect on the course of AD. Based on a PXP motif, proven to bind to the WW domain of Fe65, a new pentapeptide was designed and tested. The impedimental effect of P33 on the production of beta amyloid (A beta) (soluble fraction and aggregated plaques) and on the typical features of the AD pathology (decreased dendritic spine density, synaptic markers, elevated inflammatory reactions) was also demonstrated. Significant enhancements of both learning ability and memory function were observed in a Morris water maze paradigm. The results led us to formulate the theory that P33 acts by altering the conformation of Fe65 via binding to its WW domain, consequently hindering any interactions between Fe65 and key members involved in APP processing. LA - English DB - MTMT ER - TY - GEN AU - Apróné Török, Ibolya AU - Seprényi, György AU - Borbély, Emőke AU - Szögi, Titanilla AU - Hegyi, Péter AU - Dobó, Endre TI - Peroxidáz alapú technika alkalmazása nukleáris és citoplazmatikus antigének egymás melletti kimutatására fény- és fluoreszcens mikroszkópiában PY - 2018 UR - https://m2.mtmt.hu/api/publication/30433688 ID - 30433688 N1 - [Poszter] LA - Hungarian DB - MTMT ER - TY - JOUR AU - Gera, János AU - Szögi, Titanilla AU - Bozsó, Zsolt AU - Fülöp, Lívia AU - Barrera, Exequiel E AU - Rodriguez, Ana M AU - Méndez, Luciana AU - Delpiccolo, Carina ML AU - Mata, Ernesto G AU - Cioffi, Federica AU - Broersen, Kerensa AU - Paragi, Gábor AU - Enriz, Ricardo D TI - Searching for improved mimetic peptides inhibitors preventing conformational transition of amyloid-β42 monomer JF - BIOORGANIC CHEMISTRY J2 - BIOORG CHEM VL - 81 PY - 2018 SP - 211 EP - 221 PG - 11 SN - 0045-2068 DO - 10.1016/j.bioorg.2018.08.018 UR - https://m2.mtmt.hu/api/publication/3405755 ID - 3405755 AB - A series of novel mimetic peptides were designed, synthesised and biologically evaluated as inhibitors of Aβ42 aggregation. One of the synthesised peptidic compounds, termed compound 7 modulated Aβ42 aggregation as demonstrated by thioflavin T fluorescence, acting also as an inhibitor of the cytotoxicity exerted by Aβ42 aggregates. The early stage interaction between compound 7 and the Aβ42 monomer was investigated by replica exchange molecular dynamics (REMD) simulations and docking studies. Our theoretical results revealed that compound 7 can elongate the helical conformation state of an early stage Aβ42 monomer and it helps preventing the formation of β-sheet structures by interacting with key residues in the central hydrophobic cluster (CHC). This strategy where early “on-pathway” events are monitored by small molecules will help the development of new therapeutic strategies for Alzheimer’s disease. LA - English DB - MTMT ER - TY - JOUR AU - Olajos, Gábor AU - Hetényi, Anasztázia AU - Wéber, Edit AU - Szögi, Titanilla AU - Fülöp, Lívia AU - Martinek, Tamás TI - Peripheral cyclic β-amino acids balance the stability and edge-protection of β-sandwiches JF - ORGANIC & BIOMOLECULAR CHEMISTRY J2 - ORG BIOMOL CHEM VL - 16 PY - 2018 IS - 30 SP - 5492 EP - 5499 PG - 8 SN - 1477-0520 DO - 10.1039/c8ob01322e UR - https://m2.mtmt.hu/api/publication/3399101 ID - 3399101 N1 - Funding text: This work was supported by the Hungarian Academy of Sciences, Lendulet program (LP-2011-009) and GINOP-2.3.3-15-2016-00010. E. W. thanks the Postdoctoral Fellowship Program 2014 of the Hungarian Academy of Sciences. AB - Engineering water-soluble stand-alone beta-sandwich mimetics is a current challenge because of the difficulties associated with tailoring long-range interactions. In this work, single cis-(1R,2S)-2-aminocyclohexanecarboxylic acid mutations were introduced into the edge strands of the eight-stranded beta-sandwich mimetic structures from the betabellin family. Temperature-dependent NMR and CD measurements, together with thermodynamic analyses, demonstrated that the modified peripheral strands exhibited an irregular and partially disordered structure but were able to exert sufficient shielding on the hydrophobic core to retain the predominantly beta-sandwich structure. Although the frustrated interactions decreased the free energy of unfolding, the temperature of the maximum stabilities increased to or remained at physiologically relevant temperatures. We found that the irregular peripheral strands were able to prevent edge-to-edge association and fibril formation in the aggregation-prone model. These findings establish a beta-sandwich stabilization and aggregation inhibition approach, which does not interfere with the pillars of the peptide bond or change the net charge of the peptide. LA - English DB - MTMT ER -