TY - GEN AU - Bognár, Zita AU - Bognár, Rita AU - Ramadan, Fadi AU - Sümegi, Balázs TI - Egy ismert gyógyszermetabolit, a Desethylamiodarone potenciális szerepe az invazív hólyagdaganatok kezelésében PY - 2022 UR - https://m2.mtmt.hu/api/publication/33094535 ID - 33094535 LA - Hungarian DB - MTMT ER - TY - JOUR AU - Horváth, Orsolya AU - Takács-Ördög, Katalin AU - Bruszt, Kitti AU - Deres, László AU - Gallyas, Ferenc AU - Sümegi, Balázs AU - Tóth, Kálmán AU - Halmosi, Róbert TI - BGP-15 Protects against Heart Failure by Enhanced Mitochondrial Biogenesis and Decreased Fibrotic Remodelling in Spontaneously Hypertensive Rats JF - OXIDATIVE MEDICINE AND CELLULAR LONGEVITY J2 - OXID MED CELL LONGEV VL - 2021 PY - 2021 PG - 13 SN - 1942-0900 DO - 10.1155/2021/1250858 UR - https://m2.mtmt.hu/api/publication/31840534 ID - 31840534 N1 - Funding Agency and Grant Number: Hungarian National Research Foundations Grant [GINOP-2.3.2-15-2016-00048, GINOP 2.3.2-15-2016-00049]; NKFIH in Hungary of University of Pecs [2020-4.1.1-TKP2020] Funding text: This study was supported by the Hungarian National Research Foundations Grant (GINOP-2.3.2-15-2016-00048, GINOP 2.3.2-15-2016-00049) and NKFIH in Hungary, within the framework of the 2020-4.1.1-TKP2020 1st thematic programme of the University of Pecs. (2020-4.1.1-TKP2020). LA - English DB - MTMT ER - TY - JOUR AU - Veres, Balázs AU - Erős, Krisztián AU - Antus, Csenge Petra AU - Kálmán, Nikoletta AU - Fónai, Fruzsina AU - Jakus, Péter AU - Boros, Éva AU - Hegedűs, Zoltán AU - Nagy, István AU - Tretter, László AU - Gallyas, Ferenc AU - Sümegi, Balázs TI - Cyclophilin D-dependent mitochondrial permeability transition amplifies inflammatory reprogramming in endotoxemia JF - FEBS OPEN BIO J2 - FEBS OPEN BIO VL - 11 PY - 2021 IS - 3 SP - 684 EP - 704 PG - 21 SN - 2211-5463 DO - 10.1002/2211-5463.13091 UR - https://m2.mtmt.hu/api/publication/31822211 ID - 31822211 AB - Microorganisms or LPS (lipopolysaccharide), an outer membrane component of Gram-negative bacteria, can induce a systemic inflammatory response that leads to sepsis, multiple organ dysfunction, and mortality. Here, we investigated the role of cyclophilin D (CypD)-dependent mitochondrial permeability transition (mPT) in the immunosuppressive phase of LPS-induced endotoxic shock. The liver plays an important role in immunity and organ dysfunction; therefore, we used liver RNA sequencing (RNAseq) data, Ingenuity® Pathway Analysis (IPA ® ) to investigate the complex role of mPT formation in inflammatory reprogramming and disease progression. LPS induced significant changes in the expression of 2844 genes, affecting 179 pathways related to mitochondrial dysfunction, defective oxidative phosphorylation, nitric oxide (NO) and reactive oxygen species (ROS) accumulation, nuclear factor, erythroid 2 like 2 (Nrf2), Toll-like receptors (TLRs), and tumor necrosis factor α receptor (TNFR)-mediated processes in wild-type mice. The disruption of CypD reduced LPS-induced alterations in gene expression and pathways involving TNFRs and TLRs, in addition to improving survival and attenuating oxidative liver damage and the related NO- and ROS-producing pathways. CypD deficiency diminished the suppressive effect of LPS on mitochondrial function, nuclear- and mitochondrial-encoded genes, and mitochondrial DNA (mtDNA) quantity, which could be critical in improving survival. Our data propose that CypD-dependent mPT is an amplifier in inflammatory reprogramming and promotes disease progression. The mortality in human sepsis and shock is associated with mitochondrial dysfunction. Prevention of mPT by CypD disruption reduces inflammatory reprogramming, mitochondrial dysfunction, and lethality; therefore, CypD can be a novel drug target in endotoxic shock and related inflammatory diseases. LA - English DB - MTMT ER - TY - GEN AU - Bognár, Zita AU - Cseh, Anna Mária AU - Fekete, Katalin AU - Antus, Csenge Petra AU - Bognár, Rita AU - Tapodi, Antal AU - Ramadan, Fadi AU - Sümegi, Balázs AU - Gallyas, Ferenc TI - Amiodarone’s major metabolite, desethylamiodarone inhibits proliferation and in vivo metastasizing property of B16-F10 melanoma cells PY - 2020 UR - https://m2.mtmt.hu/api/publication/33094592 ID - 33094592 LA - English DB - MTMT ER - TY - JOUR AU - Gál, Roland AU - Deres, László AU - Horváth, Orsolya AU - Erős, Krisztián AU - Sándor, Barbara AU - Urbán, Péter AU - Soós, Szilvia AU - Márton, Zsolt AU - Sümegi, Balázs AU - Tóth, Kálmán AU - Habon, Tamás AU - Halmosi, Róbert TI - Resveratrol Improves Heart Function by Moderating Inflammatory Processes in Patients with Systolic Heart Failure JF - ANTIOXIDANTS J2 - ANTIOXIDANTS-BASEL VL - 9 PY - 2020 IS - 11 PG - 19 SN - 2076-3921 DO - 10.3390/antiox9111108 UR - https://m2.mtmt.hu/api/publication/31659630 ID - 31659630 N1 - * Megosztott szerzőség LA - English DB - MTMT ER - TY - JOUR AU - Bognár, Zita AU - Cseh, Anna Mária AU - Fekete, Katalin AU - Antus, Csenge Petra AU - Bognár, Rita AU - Tapodi, Antal AU - Ramadan, Fadi AU - Sümegi, Balázs AU - Gallyas, Ferenc TI - Amiodarone's major metabolite, desethylamiodarone inhibits proliferation of B16-F10 melanoma cells and limits lung metastasis formation in an in vivo experimental model JF - PLOS ONE J2 - PLOS ONE VL - 15 PY - 2020 IS - 9 PG - 16 SN - 1932-6203 DO - 10.1371/journal.pone.0239088 UR - https://m2.mtmt.hu/api/publication/31617910 ID - 31617910 N1 - Funding Agency and Grant Number: Hungarian grants [GINOP-2.3.3-15-2016-00025, GINOP-2.3.2-15-2016-00049, EFOP-3.6.1-16-2016-00004]; Higher Education Institutional Excellence Program Funding text: This research was funded by Hungarian grants GINOP-2.3.3-15-2016-00025, GINOP-2.3.2-15-2016-00049, EFOP-3.6.1-16-2016-00004, and Higher Education Institutional Excellence Program. Grants were received by authors BS and FGJ. The funders had no role in study design, data collection and decision to publish, or preparation of the manuscript. AB - Previously, we demonstrated the in vitro anti-tumor effects of desethylamiodarone (DEA) in bladder and cervix cancer cell lines. In the present study, we intended to establish its potentiality in B16-F10 metastatic melanoma cells in vitro and in vivo. We assessed cell proliferation, apoptosis and cell cycle by using sulforhodamine B assay, Muse™ Annexin V & Dead Cell and Muse® Cell Cycle assays, respectively. We determined colony formation after crystal violet staining. For studying mechanistic aspects, immunoblotting analysis was performed. We used a C57BL/6 experimental lung metastasis model for demonstrating in vivo anti-metastatic potential of DEA. DEA inhibited in vitro proliferation and colony formation, and in vivo lung metastasizing properties of B16-F10 cells. It arrested the cells in G0/G1 phase of their cycle likely via p21 in a p53-dependent fashion, and induced caspase mediated apoptosis likely via inversely regulating Bcl-2 and Bax levels, and reducing Akt and ERK1/2 activation. In this study, we provided in vitro and in vivo experimental evidences for DEA's potentiality in the therapy of metastatic melanomas. Since DEA is the major metabolite of amiodarone, a worldwide used antiarrhythmic drug, safety concerns could be resolved more easily for it than for a novel pharmacological agent. LA - English DB - MTMT ER - TY - JOUR AU - Gallyas, Ferenc AU - Sümegi, Balázs TI - Mitochondrial Protection by PARP Inhibition JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 21 PY - 2020 IS - 8 PG - 25 SN - 1661-6596 DO - 10.3390/ijms21082767 UR - https://m2.mtmt.hu/api/publication/31288947 ID - 31288947 AB - Inhibitors of the nuclear DNA damage sensor and signalling enzyme poly(ADP-ribose) polymerase (PARP) have recently been introduced in the therapy of cancers deficient in double-strand DNA break repair systems, and ongoing clinical trials aim to extend their use from other forms of cancer non-responsive to conventional treatments. Additionally, PARP inhibitors were suggested to be repurposed for oxidative stress-associated non-oncological diseases resulting in a devastating outcome, or requiring acute treatment. Their well-documented mitochondria- and cytoprotective effects form the basis of PARP inhibitors' therapeutic use for non-oncological diseases, yet can limit their efficacy in the treatment of cancers. A better understanding of the processes involved in their protective effects may improve the PARP inhibitors' therapeutic potential in the non-oncological indications. To this end, we endeavoured to summarise the basic features regarding mitochondrial structure and function, review the major PARP activation-induced cellular processes leading to mitochondrial damage, and discuss the role of PARP inhibition-mediated mitochondrial protection in several oxidative stress-associated diseases. LA - English DB - MTMT ER - TY - JOUR AU - Gallyas, Ferenc AU - Sümegi, Balázs AU - Szabo, Csaba TI - Role of Akt Activation in PARP Inhibitor Resistance in Cancer JF - CANCERS J2 - CANCERS VL - 12 PY - 2020 IS - 3 PG - 20 SN - 2072-6694 DO - 10.3390/cancers12030532 UR - https://m2.mtmt.hu/api/publication/31202699 ID - 31202699 N1 - Department of Biochemistry and Medical Chemistry, University of Pecs Medical School, Pecs, 7624, Hungary Szentagothai Research Centre, University of Pcs, Pecs, 7624, Hungary HAS-UP Nuclear-Mitochondrial Interactions Research Group, Budapest, 1245, Hungary Department of Medicine, University of Fribourg, Fribourg, 1700, Switzerland Cited By :53 Export Date: 5 December 2023 Correspondence Address: Gallyas, F.; Department of Biochemistry and Medical Chemistry, Hungary; email: ferenc.gallyas@aok.pte.hu AB - Poly(ADP-ribose) polymerase (PARP) inhibitors have recently been introduced in the therapy of several types of cancers not responding to conventional treatments. However, de novo and acquired PARP inhibitor resistance is a significant limiting factor in the clinical therapy, and the underlying mechanisms are not fully understood. Activity of the cytoprotective phosphatidylinositol-3 kinase (PI3K)-Akt pathway is often increased in human cancer that could result from mutation, expressional change, or amplification of upstream growth-related factor signaling elements or elements of the Akt pathway itself. However, PARP-inhibitor-induced activation of the cytoprotective PI3K-Akt pathway is overlooked, although it likely contributes to the development of PARP inhibitor resistance. Here, we briefly summarize the biological role of the PI3K-Akt pathway. Next, we overview the significance of the PARP-Akt interplay in shock, inflammation, cardiac and cerebral reperfusion, and cancer. We also discuss a recently discovered molecular mechanism that explains how PARP inhibition induces Akt activation and may account for apoptosis resistance and mitochondrial protection in oxidative stress and in cancer. LA - English DB - MTMT ER - TY - JOUR AU - Sarnyai, Farkas AU - Szekerczés, Tímea AU - Csala, Miklós AU - Sümegi, Balázs AU - Szarka, András AU - Schaff, Zsuzsa AU - Mandl, József TI - BGP-15 Protects Mitochondria in Acute, Acetaminophen Overdose Induced Liver Injury JF - PATHOLOGY AND ONCOLOGY RESEARCH J2 - PATHOL ONCOL RES VL - 26 PY - 2020 IS - 3 SP - 1797 EP - 1803 PG - 7 SN - 1219-4956 DO - 10.1007/s12253-019-00721-1 UR - https://m2.mtmt.hu/api/publication/30900106 ID - 30900106 N1 - * Megosztott szerzőség AB - Acetaminophen (APAP) induced hepatotoxicity involves activation of c-Jun amino-terminal kinase (JNK), mitochondrial damage and ER stress. BGP-15, a hydroximic acid derivative, has been reported to have hepatoprotective effects in APAP overdose induced liver damage. Effect of BGP-15 was further investigated on mitochondria in APAP-overdose induced acute liver injury in mice. We found that BGP-15 efficiently preserved mitochondrial morphology, and it caused a marked decrease in the number of damaged mitochondria. Attenuation of mitochondrial damage by BGP-15 is supported by immunohistochemistry as the TOMM20 label and the co-localized autophagy markers detected in the livers of APAP-treated mice were markedly reduced upon BGP-15 administration. This effect, along with the observed prevention of JNK activation likely contribute to the mitochondrial protective action of BGP-15. LA - English DB - MTMT ER - TY - JOUR AU - Tapody, Réka Orsolya AU - Törőcsik, Tünde AU - Fekete, István AU - Sümegi, Balázs AU - Sümegi, Pál TI - Distribution and movement of water–soluble geochemical elements in a peat bog during environmental changes and human impacts in the Eastern Carpathians in Romania. Egy tőzegláp vízoldható geokémiai elemeinek eloszlása és mozgása a környezeti változások és emberi hatások tükrében, a Keleti-Kárpátokban TS - Egy tőzegláp vízoldható geokémiai elemeinek eloszlása és mozgása a környezeti változások és emberi hatások tükrében, a Keleti-Kárpátokban JF - ARCHEOMETRIAI MŰHELY J2 - ARCHEOMETRIAI MŰHELY VL - 16 PY - 2019 IS - 3 SP - 205 EP - 213 PG - 9 SN - 1786-271X UR - https://m2.mtmt.hu/api/publication/31279224 ID - 31279224 LA - English DB - MTMT ER -